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Objectives: Dietary strategies to improve arachidonic acid:eicosapentaenoic acid (AA:EPA) ratios are of interest due to potential reductions in inflammation and oxidative stress following exercise. The aim of this study was to investigate the impact of a novel dietary intervention, that is, the ingestion of 30 g of dark chocolate, on blood lipid profiles and gut microbiota composition in elite male soccer players. Methods: Professional male soccer players were randomly assigned to the experimental group (DC) provided with 30 g of dark chocolate or to the control group (WC), provided with 30 g of white chocolate, for 30 days. Before and after intervention, blood, fecal sample, and anthropometry data were collected. For each outcome, two-way repeated-measure analysis of variance was used to identify differences between baseline and endpoint (Week 4), considering treatment (dark chocolate, white chocolate) as intersubjects' factors. Metagenomic analysis was performed following the general guidelines, which relies on the bioBakery computational environment. Results: DC group showed increased plasma polyphenols (from 154.7 ± 18.6 μg gallic acid equivalents/ml to 185.11 ± 57.6 μg gallic acid equivalents/ml, Δ pre vs. post = +30.41 ± 21.50) and significant improvements in lipid profiles: total cholesterol (Δ −32.47 ± 17.18 mg/dl DC vs. Δ −2.84 ± 6.25 mg/dl WC, Time × Treatment interaction p <.001), triglycerides (Δ −6.32 ± 4.96 mg/dl DC vs. Δ −0.42 ± 6.47 mg/dl WC, Time × Treatment interaction p <.001), low-density lipoprotein (Δ −18.42 ± 17.13 mg/dl vs. Δ −2.05 ± 5.19 mg/dl WC, Time × Treatment interaction p <.001), AA/EPA ratio (Δ −5.26 ± 2.35; −54.1% DC vs. Δ −0.47 ± 0.73, −6.41% WC, Time × Treatment interaction p <.001) compared with WC group. In addition, 4 weeks of intervention showed a significant increase in high-density lipoprotein concentration in DC group (Δ + 3.26 ± 4.49 mg/dl DC vs. Δ −0.79 ± 5.12 mg/dl WC). Microbial communities in the DC group maintained a slightly higher microbial stability over time (exhibiting lower within-subject community dissimilarity). Conclusion: Ingesting 30 g of dark chocolate over 4 weeks positively improved AA:EPA ratio and maintained gut microbial stability. Dark chocolate ingestion represents an effective nutritional strategy to improve blood lipid profiles in professional soccer players. What Are the Findings? Ingesting 30 g of dark chocolate for 4 weeks positively influences blood lipid AA: EPA ratio while maintaining gut microbial stability. What This Study Adds? Dietary intake of specific foods such as dark chocolate represents an alternative strategy to support the health and recovery of elite soccer players. WhatImpact Might This Have on Clinical Practice in the Future? From a clinical and translational perspective, dark chocolate ingestion positively modulates favorable blood lipid profiles and polyunsaturated fatty acid metabolism while maintaining gut microbial stability. Dark chocolate ingestion may be considered as an effective nutritional strategy in elite sport environments during periods of high-intensity training and congested competitions. Further research is required to determine functional outcomes associated with the observed improvements in blood lipid profiles. [ABSTRACT FROM AUTHOR]

Deep learning is evolving in nutritional epidemiology to address challenges including precise nutrition and data-driven disease modeling. Fermented dairy products consumption as the implementation of specific dietary priority contributes to a lower risk of all-cause mortality, cardiovascular disease, and obesity. Various lipid types play different roles in cardiometabolic health and fermentation process changes the lipid profile in dairy products. Leveraging the power of multiple biological datasets can provide mechanistic insights into how proteins impact lipid pathways, and establish connections among fermentation-lipid biomarkers-protein. The recent leap of deep learning has been performed in food category recognition, agro-food freshness detection, and food flavor prediction and regulation. The proposed multimodal deep learning method includes four steps: (i) Forming data matrices based on data generated from different omics layers. (ii) Decomposing high-dimensional omics data according to self-attention mechanism. (iii) Constructing View Correlation Discovery Network to learn the cross-omics correlations and integrate different omics datasets. (iv) Depicting a biological network for lipid metabolism-centered quantitative multi-omics data analysis. Relying on the cytidine diphosphate-diacylglycerol synthase-mediated lipid metabolism regulates the glycerophospholipid composition of fermented dairy effectively. Innovative processing strategies including ohmic heating and pulsed electric field improve the sensory qualities and nutritional characteristics of the products. [ABSTRACT FROM AUTHOR]

As far as health benefit is concerned, dark tea is one of the best beverages in the world. Theabrownins are the major ingredient contributing to the health benefits of dark tea and known as "the soft gold in dark tea." A growing body of evidence indicated that theabrownins are macromolecular pigments with reddish-brown color and mellow taste, and mainly derived from the oxidative polymerization of tea polyphenols. Theabrownins are the main active ingredients in dark tea which brings multiple health-promoting effects in modulating lipid metabolism, reducing body weight gain, attenuating diabetes, mitigating NAFLD, scavenging ROS, and preventing tumors. More importantly, it's their substantial generation in microbial fermentation that endows dark tea with much stronger hypolipidemic effect compared with other types of tea. This review firstly summarizes the most recent findings on the preparation, structural characteristics, and health-promoting effects of theabrownins, emphasizing the underlying molecular mechanism, especially the different mechanisms behind the effect of theabrownins-mediated gut microbiota on the host's multiple health-promoting benefits. Furthermore, this review points out the main limitations of current research and potential future research directions, hoping to provide updated scientific evidence for their better theoretical research and industrial utilization. [ABSTRACT FROM AUTHOR]

Psoriasis is a kind of severe immune-mediated systemic skin disorder, becoming a worldwide public health concern. Daturataturin A (DTA), a withanolide compound, exerts excellent anti-inflammatory and anti-proliferative properties. The objective of this study is to elucidate the effect of DTA on psoriasis and its potential mechanism. We established psoriasis-like keratinocytes model by stimulating HaCaT cells with M5 cocktail cytokines including Interleukin (IL)-17A, IL-22, oncostatin M, IL-1α, and tumor necrosis factor-α (TNF-α), followed by intervention with DTA. The potential effects and mechanisms of DTA on psoriasis were evaluated in vitro. DTA was found to be able to inhibit hyperproliferation, promote apoptosis, decrease the release of pro-inflammatory cytokines, downregulate keratin expression, and improve lipid metabolism via regulating the peroxisome proliferator-activated receptor (PPAR) signaling pathway by M5 cocktail cytokines stimulation in HaCaT cells. DTA ameliorated lipid metabolism of psoriasis and exerted the potential anti-psoriasis effects by regulating PPAR pathway in vitro, suggesting that DTA may act as a new therapeutic agent for psoriasis. [ABSTRACT FROM AUTHOR]

The list of standard abbreviations for JDS is available at adsa.org/jds-abbreviations-24. Nonstandard abbreviations are available in the Notes. The study examined how dietary milk polar lipids affect gut permeability, systemic inflammation, and lipid metabolism during diet-induced obesity (DIO). C57BL/6J mice (n = 6 × 3) were fed different diets with 34% fat as energy for 15 wk: (1) a modified AIN-93G diet (control; CO); (2) CO with milk gangliosides (GG); and (3) CO with milk phospholipids (MPL). Gut permeability was assessed by fluorescein isothiocyanate-dextran and sugar absorption tests. Intestinal tight junction proteins were evaluated by western blot. Plasma cytokines were measured by immunoassay. Body composition was assessed by magnetic resonance imaging. Tissue lipid profiles were obtained by thin layer chromatography. Hepatic expression of genes associated with lipid metabolism was assessed by real-time quantitative PCR. The MPL diet increased the efficiency of converting food into body fat and facilitated body fat accumulation compared with CO. The MPL and GG diets did not affect fasting glucose or the homeostasis model assessment of insulin resistance during DIO. The MPL diet increased and GG decreased plasma triglycerides compared with CO. The MPL diet decreased phospholipids subclasses in the muscle and increased those in the liver compared with CO. The GG and MPL diets had little effect on hepatic expression of genes associated with lipid metabolism. Compared with CO, the MPL diet decreased polar lipids content in colon mucosa. Small intestinal permeability decreased, whereas colon permeability increased and then recovered during the feeding period. High-fat feeding increased plasma endotoxin after DIO but did not affect plasma cytokines. The MPL and GG diets did not affect plasma endotoxin, adipokines, and inflammatory cytokines. After the establishment of obesity, MPL increased gut permeability to large molecules but decreased intestinal absorption of small molecules, whereas GG tended to have the opposite effects. The MPL and GG diets decreased mannitol and sucralose excretions, which peaked at d 45 in the CO group. The MPL diet decreased occludin in jejunum mucosa compared with CO. The GG and MPL diets did not affect zonula occludens-1 in gut mucosa. Overall, during DIO, milk GG decreased gut permeability, and had little effect on systemic inflammation and lipid metabolism; MPL facilitated body fat accumulation, decreased gut permeability, did not affect systemic inflammation. [Display omitted] [ABSTRACT FROM AUTHOR]

Objective: The inconsistency in conclusions from early observational studies has sparked our interest in elucidating the relationship between lipid levels and susceptibility to hyperemesis gravidarum (HG). This study wishes to employed Mendelian randomization analysis to investigate the causal relationship between low-density lipoprotein cholesterol (LDL-C) and HG. Methods: We employed Tow-Sample MR analysis to investigate the causal associations between LDL-C and HG. Specific variables were selected from GWAS database for MR analysis, using single nucleotide polymorphisms (SNPs) as our instruments. The threshold for significant SNPs as genetic instruments has been set at 5 × 10−8. F-statistic was employed to validate the strength of exposure instruments. The causality was mainly evaluated by Inverse Variance Weighted method (IVW). To address potential bias from the selection of genetic variants with pleiotropic effects, sensitivity analysis was performed by Cochrane Q-test, MR Egger, weighted median, MR-PRESSO and Leave-one-out methods. To validate the directionality of causal relationships, we employed Steiger test to filter SNPs. At last, we conducted reverse MR to exclude the causal impact of HG on LDL-C levels. Results: Our MR results identified the effect of genetically predicted increased LDL-C levels on increased genetic susceptibility to HG (OR:1.30; 95%CI:1.03-1.65; p = 0.028). In reverse MR analyses, no evidence was found for causal effect of HG on LDL-C levels (OR:1.00; 95%CI:1.00-1.01; p = 0.163). Sensitivity analyses were used to confirm reliability. Conclusion: This study may have provided evidence of genetically predicted increased LDL-C levels on increased genetic susceptibility to HG. Appropriate lowering LDL-C levels may serve as a preventive and treatment measure for HG. [ABSTRACT FROM AUTHOR]

• PCPE-1 and PCPE-2 share high structural similarity. • PCPE-2 is described as an enhancer of collagen proteolytic maturation like PCPE-1. • PCPE-2 differs from PCPE-1 by its ability to inhibit BMP-1 and tolloid proteinases. • The two proteins have different expression patterns in normal and disease tissues. • PCPE-2 also regulates lipid metabolism and innate immunity. PCPE-2 was discovered at the beginning of this century, and was soon identified as a close homolog of PCPE-1 (procollagen C-proteinase enhancer 1). After the demonstration that it could also stimulate the proteolytic maturation of fibrillar procollagens by BMP-1/tolloid-like proteinases (BTPs), PCPE-2 did not attract much attention as it was thought to fulfill the same functions as PCPE-1 which was already well-described. However, the tissue distribution of PCPE-2 shows both common points and significant differences with PCPE-1, suggesting that their activities are not fully overlapping. Also, the recently established connections between PCPE-2 (gene name PCOLCE2) and several important diseases such as atherosclerosis, inflammatory diseases and cancer have highlighted the need for a thorough reappraisal of the in vivo roles of this regulatory protein. In this context, the recent finding that, while retaining the ability to bind fibrillar procollagens and to activate their C-terminal maturation, PCPE-2 can also bind BTPs and inhibit their activity has substantially extended its potential functions. In this review, we describe the current knowledge about PCPE-2 with a focus on collagen fibrillogenesis, lipid metabolism and inflammation, and discuss how we could further advance our understanding of PCPE-2-dependent biological processes. [ABSTRACT FROM AUTHOR]

Macrophage polarization is increasingly recognized as a vital pathogenetic factor in Crohn's disease (CD). Adropin is a secreted protein implicated in energy homeostasis, chiefly linked to glucose and lipid metabolism. However, the significance of adropin in CD is not clear. The objective of this study was to detect the expression of adropin in CD patients and investigate the effect of adropin on macrophage polarization induced by lipopolysaccharide (LPS) and its potential mechanism. Our study showed that serum adropin levels were markedly lower in patients with CD in active (CDA) than patients with CD in remission (CDR) and control groups (p < 0.01), however, there was no significant difference between in remission CD and healthy controls (p > 0.05). The colon mucous adropin levels in CDA were distinctly higher than CDR and controls (p < 0.01), while a significant difference between in remission CD and in healthy controls was not observed (p > 0.05). Exploration of the specific mechanism of action indicated that adropin promoted LPS‐induced RAW264.7 macrophage polarization to M2 phenotype by modulating the expression and nuclear translocation of peroxisome proliferator receptor gamma (PPARγ), which may help weaken the intestinal inflammatory response. PPARγ inhibitor GW9662 reversed adropin‐induced M2 macrophage polarization. Knockdown of GPR19, an adropin receptor, abrogated the M2 macrophage polarization caused by PPARγ. These findings suggest that adropin in colonic mucosa is a protective response in patients with active Crohn's disease. [ABSTRACT FROM AUTHOR]

PURPOSE: Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect of cytotoxic cancer treatment, often necessitating dose reduction (DR) or chemotherapy discontinuation (CD). Studies on peripheral neuropathy related to chemotherapy, obesity, and diabetes have implicated lipid metabolism. This study examined the association between circulating lipids and CIPN. METHODS: Lipidomic analysis was performed on plasma samples from 137 patients receiving taxane-based treatment. CIPN was graded using Total Neuropathy Score-clinical version (TNSc) and patient-reported outcome measure European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-CIPN (EORTC-QLQ-CIPN20). RESULTS: A significant proportion of elevated baseline lipids were associated with high-grade CIPN defined by TNSc and EORTC-QLQ-CIPN20 including triacylglycerols (TGs). Multivariable Cox regression on lipid species, adjusting for BMI, age, and diabetes, showed several elevated baseline TG associated with shorter time to DR/CD. Latent class analysis identified two baseline lipid profiles with differences in risk of CIPN (hazard ratio, 2.80 [95% CI, 1.50 to 5.23]; P =.0013). The higher risk lipid profile had several elevated TG species and was independently associated with DR/CD when modeled with other clinical factors (diabetes, age, BMI, or prior numbness/tingling). CONCLUSION: Elevated baseline plasma TG is associated with an increased risk of CIPN development and warrants further validation in other cohorts. Ultimately, this may enable therapeutic intervention. [ABSTRACT FROM AUTHOR]

Regression of cirrhosis has been observed in patients with viral and non-viral etiologies of liver disease in whom the underlying cause of liver injury was effectively suppressed. However, the understanding of the factors contributing to reversibility of fibrosis and cirrhosis is limited. Our aims were to assess clinical factors, perform genotyping of known variants, and comprehensive metabolic phenotyping to characterize the regression of fibrosis in patients with compensated advanced chronic liver disease (cACLD). In a case-control pilot study of 81 patients with cACLD, we compared individuals exhibiting histological or clinical evidence of cACLD regression ("regressors"; n = 44) with those showing no improvement ("non-regressors"; n = 37) after a minimum of 24 months of successful treatment of the cause of liver disease. Data were validated using an external validation cohort (n = 30). Regardless of the cause of cACLD, the presence of obesity (odds ratio [OR] 0.267 95% CI 0.072-0.882; p = 0.049), high liver stiffness (OR 0.960, 95% CI 0.925-0.995; p = 0.032), and carriage of GCKR variant rs1260326 (OR 0.148, 95% CI 0.030-0.773; p = 0.019) are associated with a reduced likelihood of fibrosis regression in a subgroup of 60 patients with ACLD genotyped for known genetic variants. Using liver tissue transcriptomics, we identified metabolic pathways differentiating regressors from non-regressors, with top pathways associated with lipid metabolism – especially fatty acids, bile acids, phospholipids, triacylglycerides (biosynthesis), and the carnitine shuttle. In the entire discovery cohort, we further measured metabolites within the defined pathways, which led to the identification of 33 circulating markers differentiating regressors from non-regressors after etiological therapy. The validation cohort confirmed 14 of the differentially expressed markers. We identified and validated a group of lipid biomarkers associated with regression of fibrosis that could be used as non-invasive biomarkers for detecting regression of fibrosis in cACLD. Regression of cirrhosis/advanced chronic liver disease (ACLD) after removal of the underlying cause of liver injury has been observed in human cirrhosis. However, detailed characterization of ACLD regression remains an unmet need. In this study, we provide a comprehensive phenotyping of individuals likely to experience ACLD regression. While obesity, carriage of GCKR variant rs1260326 and high liver stiffness were associated with lower likelihood of regression of ACLD, a signature of circulating lipid metabolites enabled differentiation of regressors from non-regressors after effective etiologic therapy. The lipid signature we discovered and externally validated could be used as non-invasive biomarker to detect regression of fibrosis in patients with compensated ACLD. [Display omitted] • We demonstrate that fibrosis regression of cACLD is shaped by a multifaceted interplay of clinical, genetic, and metabolic factors. • Obesity, high LSM and carrying the rs1260326 variant of GCKR were associated with a lower probability of fibrosis regression. • Metabolomics revealed lipid perturbations associated with fibrosis regression, with taurocholic and taurochenodeoxycholic acid emerging as key predictors. • We identified a lipid signature associated with regression of ACLD that could be used as a non-invasive biomarker. [ABSTRACT FROM AUTHOR]

Self‐ and other‐directed compassion have been linked with better mental and physical health but research on factors contributing to their development is scarce. Previous studies indicate a possible causal relationship of lipids with personality and socioemotional functioning. As an extension to earlier research, in the present study we examine whether lipids assessed in adolescence and adulthood are associated with self‐compassion and other‐directed compassion in adulthood. The study utilizes data on lipids from two follow‐ups in the Northern Finland Birth Cohort 1986 at ages 15–16 and 33–35. In the latter follow‐up also self‐compassion and other‐directed compassion were assessed with the self‐compassion scale – short form and the subscale for compassion in the dispositional positive emotions scale, respectively. The sample for the cross‐sectional associations of lipids in adulthood with the compassion variables in adulthood includes 1,459 participants, whereas the sample for the longitudinal associations of lipids in adolescence and the compassion variables in adulthood consists of 1,509 participants. The associations were examined with hierarchical linear regression (lipids as continuous variables) and univariate general linear model (lipids as categorical variables). The results suggest that in women, high‐density lipoprotein (HDL) cholesterol in adolescence is associated with high empathic concern (a component of other‐directed compassion) in adulthood. The results show further that, in women, an HDL cholesterol level above 1.2 mmol/L in adulthood is associated with high other‐directed compassion and empathic concern in adulthood. The present study provides tentative evidence that biological factors such as lipids might play a role in the development of empathic concern and other‐directed compassion. [ABSTRACT FROM AUTHOR]

Metamorphosis plays an important role in the evolutionary success of insects. Accumulating evidence indicated that microRNAs (miRNAs) are involved in the regulation of processes associated with insect metamorphosis. However, the miRNAs coordinated with juvenile hormone (JH)‐regulated metamorphosis remain poorly reported. In the present study, using high‐throughput miRNA sequencing combined with Drosophila genetic approaches, we demonstrated that miR‐iab‐8, which primarily targets homeotic genes to modulate haltere‐wing transformation and sterility was up‐regulated by JH and involved in JH‐mediated metamorphosis. Overexpression of miR‐iab‐8 in the fat body resulted in delayed development and failure of larval‐pupal transition. Furthermore, metabolomic analysis results revealed that overexpression of miR‐iab‐8 caused severe energy metabolism defects especially the lipid metabolism, resulting in significantly reduced triacylglycerol (TG) content and glycerophospholipids but enhanced accumulation of phosphatidylcholine (PC) and phosphatidylethanolamine (PE). In line with this, Nile red staining demonstrated that during the third larval development, the TG content in the miR‐iab‐8 overexpression larvae was continuously decreased, which is opposite to the control. Additionally, the transcription levels of genes committed to TG synthesis and breakdown were found to be significantly increased and the expression of genes responsible for glycerophospholipids metabolism were also altered. Overall, we proposed that JH induced miR‐iab‐8 expression to perturb the lipid metabolism homeostasis especially the TG storage in the fat body, which in turn affected larval growth and metamorphosis. [ABSTRACT FROM AUTHOR]

Objective(s): Obesity leads to severe health issues like cardiovascular disease. Natural substances with anti-obesity properties are gaining attention. This study investigates the impact of taurine on lipid levels in rats fed a high-fat diet. Materials and Methods: The SD rats were fed a high-fat diet and treated with or without taurine for 21 weeks. Taurine was added to their drinking water, and an adipose triglyceride lipase (ATGL) inhibitor was injected for one week. The study evaluated the impact of taurine supplementation on the rats' body weight, Lee index, body fat content, serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), fatty acid synthase (FAS), ATGL, and peroxisome proliferator-activated receptor α (PPARα) in the liver. Fat accumulation in the liver and aortic arch was assessed through histopathological observations. Results: The study found that taurine reduced body weight, body fat, serum TG, TC, LDL-C levels, and lipid deposition in the liver and aortic arch while increasing serum HDL-C levels. Taurine intake also increased FAS and ATGL expression in the liver. Interestingly, the ATGL inhibitor atglistatin did not affect FAS and ATGL expression in the presence of taurine. Conclusion: Taurine can reduce fat deposition caused by a high-fat diet in SD rats by decreasing FAS content and increasing ATGL content. However, taurine does not fully regulate FAS and ATGL expression through the ATGL pathway. [ABSTRACT FROM AUTHOR]

This study investigated the potential role and underlying mechanisms of oleanolic acid (OA), a pentacyclic triterpene with antioxidant and anti-inflammatory properties, in porcine oocytes during in vitro maturation (IVM). The results showed that supplementation with 5 μM OA during IVM resulted in a greater percentage of mature oocytes, parthenogenetically activated embryos and somatic cell nuclear-transferred embryos. This was evidenced by significant increases in the rate of first polar body expulsion, the expansion of cumulus granulosa cells and the total cell number in blastocysts. Further analysis revealed that OA promoted fatty acid accumulation and upregulated the mRNA expression of genes involved in fatty acid β-oxidation. OA significantly increased the intracellular mitochondrial membrane potential and ATP levels and effectively inhibited BAX/BCL2 and Cleaved Caspase3 protein expression. Notably, OA increased the protein levels of intracellular Nrf2 and HO-1, and the GSH levels and the activities of the antioxidant enzymes SOD and catalase (CAT), while reducing ROS levels. Mechanistically, OA activated the Nrf2/HO-1 signalling pathway, which is crucial for regulating the expression of antioxidant-related targets in IVM porcine oocytes. Our findings indicated that OA improved antioxidant capacity by activating the Nrf2/HO-1 signalling pathway, thereby promoting porcine oocyte maturation. • Supplementation with OA during IVM promotes porcine oocyte maturation and fosters embryonic development in vitro. • OA sustains lipid metabolism in porcine oocytes. • OA elevates mitochondrial function and antioxidant capacity in porcine oocytes. • OA activated the Nrf2/HO-1 signalling pathway in porcine oocytes. [ABSTRACT FROM AUTHOR]

In understanding stress response mechanisms in fungi, cold stress has received less attention than heat stress. However, cold stress has shown its importance in various research fields. The following study examined the cold stress response of six Pseudogymnoascus spp. isolated from various biogeographical regions through a proteomic approach. In total, 2541 proteins were identified with high confidence. Gene Ontology enrichment analysis showed diversity in the cold stress response pathways for all six Pseudogymnoascus spp. isolates, with metabolic and translation-related processes being prominent in most isolates. 25.6% of the proteins with an increase in relative abundance were increased by more than 3.0-fold. There was no link between the geographical origin of the isolates and the cold stress response of Pseudogymnoascus spp. However, one Antarctic isolate, sp3, showed a distinctive cold stress response profile involving increased flavin/riboflavin biosynthesis and methane metabolism. This Antarctic isolate (sp3) was also the only one that showed decreased phospholipid metabolism in cold stress conditions. This work will improve our understanding of the mechanisms of cold stress response and adaptation in psychrotolerant soil microfungi, with specific attention to the fungal genus Pseudogymnoascus. [ABSTRACT FROM AUTHOR]

Ageing often leads to the deterioration of physiological functions, including a decline in antioxidant defences, which can result in various health complications. Exogenous antioxidants have been recognised for their potential to alleviate these age-related health complications. Virgin coconut oil (VCO), known for its antioxidant, anti-inflammatory and anti-lipidemic efficacies, has gained recognition as a functional food with promising benefits. However, the safety of VCO consumption among individuals of the aged and diseased population remains to be fully established. Five experimental groups were established, consisting of one control group and four groups administered either "2 mL" or "4 mL" per kg body weight of "HP-VCO" or "F-VCO" daily for six weeks. Body weight, water, and feed intake were monitored. After six weeks, animals were euthanized, blood and organs were collected for analysis. Oxidative stress and dyslipidemia markers were analysed, and liver tissues underwent histological examination. HP-VCO-administered animals exhibited increased serum total cholesterol and triglycerides, whereas F-VCO-fed animals showed reduced triglyceride levels. LDL-cholesterol levels decreased in all VCO-fed groups, accompanied by increased HDL-cholesterol levels. Additionally, all treated groups showed a slight increase in the HMG Co. A/mevalonate ratio. Both VCO-fed animals displayed elevated reduced glutathione levels and reduced glutathione – S transferase activity. Consistent with these findings, decreased conjugated dienes and thiobarbituric acid reactive substances confirmed the improved redox status. The study indicated that F-VCO is advantageous over VCO prepared by hot pressing as it offers protection against oxidative stress and related degenerative diseases. [Display omitted] • Regardless of its preparation mode, VCO reduces LDL-C and increases HDL-C in aged rats. • VCO promotes an endogenous antioxidant defence system in aged rats. • Studies indicate the Cardiovascular benefits of VCO and safe for the aged population. [ABSTRACT FROM AUTHOR]

The tight regulation of glucose and lipid metabolism is crucial for maintaining metabolic health. Dysregulation of these processes can lead to the development of metabolic diseases. Secreted factors, or hormones, play an essential role in the regulation of glucose and lipid metabolism, thus also playing an important role in the development of metabolic diseases such as type 2 diabetes and obesity. Given the important roles of secreted factors, there has been significant interest in identifying new secreted factors and new functions for existing secreted factors that control glucose and lipid metabolism. In this review, we evaluate novel secreted factors or novel functions of existing factors that regulate glucose and lipid metabolism discovered in the last decade, including secreted isoform of endoplasmic reticulum membrane complex subunit 10, vimentin, cartilage intermediate layer protein 2, isthmin-1, lipocalin-2, neuregulin-1 and neuregulin-4. We discuss their discovery, tissues of origin, mechanisms of action and sex differences, emphasising their potential to regulate metabolic processes central to diabetes. Additionally, we discuss the translational barriers, particularly the absence of identified receptors, that hamper their functional characterisation and further therapeutic development. Ultimately, the identification of new secreted factors may give insights into previously unidentified pathways of disease progression and mechanisms of glucose and lipid homeostasis. [ABSTRACT FROM AUTHOR]

Fibroblast growth factor 23 (FGF23) is a bone-secreted protein widely recognized as a critical regulator of skeletal and mineral metabolism. However, little is known about the nonskeletal production of FGF23 and its role in tissues other than bone. Growing evidence indicates that circulating FGF23 levels rise with a high-fat diet (HFD) and they are positively correlated with body mass index (BMI) in humans. In the present study, we show for the first time that increased circulating FGF23 levels in obese humans correlate with increased expression of adipose Fgf23 and both positively correlate with BMI. To understand the role of adipose-derived Fgf23 , we generated adipocyte-specific Fgf23 knockout mice (AdipoqFgf23Δfl/Δfl) using the adiponectin-Cre driver, which targets mature white, beige, and brown adipocytes. Our data show that targeted ablation of Fgf23 in adipocytes prevents HFD-fed female mice from gaining body weight and fat mass while preserving lean mass but has no effect on male mice, indicating the presence of sexual dimorphism. These effects are observed in the absence of changes in food and energy intake. Adipose Fgf23 inactivation also prevents dyslipidemia, hyperglycemia, and hepatic steatosis in female mice. Moreover, these changes are associated with decreased respiratory exchange ratio and increased brown fat Ucp1 expression in knockout mice compared to HFD-fed control mice (Fgf23fl/fl). In conclusion, this is the first study highlighting that targeted inactivation of Fgf23 is a promising therapeutic strategy for weight loss and lean mass preservation in humans. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effect of Sanhuang Xiexin Decoction (SXD) on triple-negative breast cancer (TNBC) in mice and its underlying mechanism. Methods: The high-performance liquid chromatography (HPLC) was used to quantitate and qualify SXD. A total of 15 female BALB/c mice were inoculated subcutaneously on the right hypogastrium with 3×105 of 4T1-Luc cells to establish TNBC mouse model. All mice were divided randomly into 3 groups, including phosphate buffered solution (PBS), SXD and doxorubicin (DOX) groups (positive drug). Additionally, tumor growth, pathological changes, serum lipid profiles, expression of Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) signaling pathway and its key targets including inflammatory factors, cell cycle and epithelial-mesenchymal transition (EMT) markers were investigated. Besides, the biosafety of SXD was also evaluated in mice. Results: Rhein, coptisine, berberine hydrochloride and baicalin were all found in SXD, and the concentrations of these 4 components were 0.57, 2.61, 2.93, and 46.04 mg/g, respectively. The mouse experiment showed that SXD could notably suppress the development of tumors and reduce the density of tumor cells (P<0.01). The serum lipid analysis and Oil-Red-O staining both showed the differences, SXD group exhibited higher serum adiponectin and HDL-C levels with lower TC and LDL-C levels compared to the PBS and DOX groups (P<0.05 or P<0.01), respectively. SXD also decreased the levels of phospho-JAK2 (p-JAK2), phospho-STAT3 (p-STAT3) expressions and its downstream factors, including mostly inflammatory cytokine, EMT markers, S phase of tumor cells and vascular endothelial growth factor (VEGF) expression (P<0.05 or P<0.01), respectively. The biosafety assessment of SXD revealed low levels of toxicity in mice. Conclusion: SXD could inhibit TNBC by suppressing JAK2-STAT3 phosphorylation which may be associated with modulation of lipid metabolism. [ABSTRACT FROM AUTHOR]

To investigate the influences of dietary protein and lipid levels on the growth, feed utilization, morphometric parameters, body composition, serum biochemical parameters, and lipid metabolism of golden pompano (Trachinotus ovatus), nine test diets containing three protein levels (35%, 40%, and 45%) and three lipid levels (8%, 13%, and 18%) were designed in the present study. Each diet (named D1–D9) was randomly assigned to feed triplicate groups of golden pompano juvenile (initial weight ~ 70 g) for 50 days. The results showed that the dietary lipid levels positively correlated with weight gain, specific growth rate, and protein efficiency ratio (PER), suggesting that the high lipid diets (18%) can be efficiently utilized in this fish species. The dietary protein levels have no significant influences on the growth and feed utilization except for the PER. Increasing dietary protein levels resulted in a decrease in hepatosomatic index (HSI), viscerosomatic index (VSI), and intestinal somatic index (ISI), while the dietary lipid level did not have a significant impact on morphological indices except for ISI. The dietary protein and lipid levels had no significant influences on the contents of crude lipid, crude ash, and moisture of whole body, while the crude protein contents was significantly affected by the dietary protein levels. Serum biochemical indexes, including cholesterol (CHO), triglycerides (TG), high-density lipoprotein cholesterol (HDL), and low-density lipoprotein cholesterol (LDL), as well as HDL/LDL ratio were significantly affected by the dietary lipid levels, but not by the dietary protein levels. The expression levels of genes and their associated proteins involved in hepatic lipogenesis (Srebp-1c and Fas) and fatty acids β-oxidation (Pparα and Cpt-1) were up-regulated with increasing dietary lipid levels, while the former was up-regulated, and the latter was down-regulated with increasing dietary protein levels. Considering the present results in terms of growth performance, feed utilization, morphometric parameters, and lipid metabolism, the recommended dietary protein and lipid levels for golden pompano are 40% and 18%, respectively. The findings suggested that this species exhibits a significant protein-sparing effect on lipid utilization. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is a prevalent malignant tumor worldwide, leading to significant morbidity and disease burden. Diagnostic indicators and treatment objectives for CRC are urgently needed. This study demonstrates that GPR37, a GPCR receptor, is highly expressed in CRC. Depletion of GPR37 significantly reduced CRC tumor cell growth both in vitro and in vivo. Further tests showed that GPR37 protects cancer cells from ferroptosis by upregulating SCD1 expression, thereby modulating lipid metabolism, suppressing the level of reactive oxygen species, and mitigating ferroptosis. Mechanistic studies have shown that GPR37 modulates lipid metabolism in tumor cells by promoting SCD1 transcription via the MAPK-p38 signaling pathway. Our results reveal the pro-carcinogenic effect of GPR37 in primary CRC and suggest that targeting GPR37 could be a potential therapeutic target for CRC. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN) is a severe complication of diabetes mellitus, causing a substantive threat to the public, which receives global concern. However, there are limited drugs targeting the treatment of DN. Owing to this, it is highly crucial to investigate the pathogenesis and potential therapeutic targets of DN. The process of ferroptosis is a type of regulated cell death (RCD) involving the presence of iron, distinct from autophagy, apoptosis, and pyroptosis. A primary mechanism of ferroptosis is associated with iron metabolism, lipid metabolism, and the accumulation of ROS. Recently, many studies testified to the significance of ferroptosis in kidney tissue under diabetic conditions and explored the drugs targeting ferroptosis in DN therapy. Our review summarized the most current studies between ferroptosis and DN, along with investigating the significant processes of ferroptosis in different kidney cells, providing a novel target treatment option for DN. [ABSTRACT FROM AUTHOR]

Background: Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear. Methods: This study included 125 male OSA subjects from the Shanghai Sleep Health Study (SSHS) who were matched for age, body mass index (BMI), and lipid profile. Serum ANGPTL4 levels were measured via ELISA. The ANGPTL4 T266M variants of 4455 subjects along with their anthropometric, fasting biochemical, and standard polysomnographic parameters were collected. Linear regression was used to analyze the associations between quantitative traits and ANGPTL4 T266M. Molecular docking and molecular dynamic simulation were employed to compare the effects of the wild-type ANGPTL4 and its T266M mutation on ACACA. Results: Serum ANGPTL4 levels significantly decreased with increasing OSA severity (non-OSA: 59.6±17.4 ng/mL, mild OSA: 50.0±17.5 ng/mL, moderate OSA: 46.3±15.5 ng/mL, severe OSA: 19.9±14.3 ng/mL, respectively, p=6.02x10-16). No associations were found between T266M and clinical characteristics. Molecular docking indicated that mutant ANGTPL4 T266M had stronger binding affinity for the ACACA protein, compared with wild-type ANGPTL4. In terms of protein secondary structure, mutant ANGTPL4 T266M demonstrated greater stability than wild-type ANGPTL4. Conclusions: Serum ANGTPL4 levels were significantly decreased in OSA patients, particularly among individuals with severe OSA. Although functional ANGTPL4 T266M variants were not associated with lipid levels in OSA, ANGTPL4 T266M could enhance binding affinity for the ACACA protein, potentially regulating lipid metabolism. [ABSTRACT FROM AUTHOR]

Bile acids (BAs) are significantly altered in the liver and serum of patients with nonalcoholic steatohepatitis (NASH). However, the underlying mechanisms of these changes, particularly BA alternative pathways (BAP) responsible for non12‐OH BAs, remain unclear. RNA‐seq data were initially analyzed to reveal the changes of gene expression in NASH patients. Targeted metabolomics were conducted on plasma from NASH mice induced by high‐fat or western diet with CCl4 for 10–24 weeks. Liver tissues were examined using proteomics, RT‐qPCR, and western blotting. An integrated approach was then employed to analyze protein interactions and network correlations. Analysis of RNA‐seq data revealed the inhibition of CYP7B1 in NASH patients, indicating the dysregulation of BAP. In NASH mouse models, dysregulation of BA circulation was observed by increased plasma total BA (TBA) levels and decreased liver TBA, with liver swelling and histopathological changes. Targeted metabolomics revealed suppressed levels of non12‐OH BAs, which inversely correlated with increased liver injury markers. The reduced mRNA and protein expression of Fxr and upregulation of Lxr signaling in livers suggested the suppressed BAP was modulated by Fxr‐Lxr signaling. Moreover, BAP interactions predominantly implicated multiple metabolism disruptions, involving 7 hub proteins (Hk1, Acadsb, Pklr, Insr, Ldlr, Cyp27a1, and Cyp7b1), offering promising therapeutic targets for NASH. We presented the metabolic and proteomic map of BAP and its regulatory network in NASH progression. Therapeutic targeting of BAP or its co‐regulatory proteins holds promise for NASH treatment and metabolic syndrome management. [ABSTRACT FROM AUTHOR]

Background: Metabolic dysfunction-associated steatosis liver disease (MASLD) is one of the most common metabolic liver diseases around the world, whose prevalence continues to increase. Currently, there are few medications to treat MASLD. Ergothioneine is a natural compound derived from mushrooms whose sulfhydryl groups confer unique antioxidant, anti-inflammatory and detoxifying effects. Currently, research on the therapeutic effects of ergothioneine in MASLD is unknown. Therefore, this study explored the effect and mechanism of EGT in MASLD. Methods: The ameliorative effects and mechanisms of ergothioneine on MASLD were evaluated using HFD mice and PA-treated AML12 cells. Mouse body weight, body fat, IPGTT, IPITT, immunohistochemistry, serum biochemical indices, and staining of liver sections were assayed to verify the protective role of ergothioneine in MASLD. RNA-seq was applied to explore the mechanism of action of ergothioneine. The role of ergothioneine in AML12 was confirmed by western blotting, qPCR, ELISA, Oil Red O staining, flow cytometry, and ROS assays. Subsequently, the 3-methyladenine (3-MA, an autophagy inhibitor) was subsequently used to confirm that ergothioneine alleviated MASLD by promoting autophagy. Results: Ergothioneine reduced body weight, body fat and blood lipids, and improved insulin resistance and lipid and glycogen deposition in MASLD mice. Furthermore, ergothioneine was found to increase autophagy levels and attenuate oxidative damage, inflammation, and apoptosis. In contrast, intervention with 3-MA abrogated these effects, suggesting that ergothioneine ameliorated effects by promoting autophagy. Conclusion: Ergothioneine may be a drug with great therapeutic potential for MASLD. Furthermore, this protective effect was mediated through the activation of autophagy. [ABSTRACT FROM AUTHOR]

Background: Perfluoroalkyl and polyfluoroalkyl substances (PFAS) exposure has been associated with metabolic diseases, however, the underlying molecular pathogenesis remains to be understood. Integrated PFAS and lipidomic analysis has the potential to identify alterations in lipid metabolism pathways for exposome research. Methods: A targeted LC-MS/MS method was developed for the quantification of 14 PFAS from human plasma samples (n = 96). Concurrently, high coverage lipidomics was conducted for the quantification of 665 lipid species in the same plasma samples. Linear regression models were implemented to study the association of PFAS with plasma lipidome. Results: Women had lower levels of PFAS compared to men and Asian-Indians had lower levels of PFAS compared to both Chinese and Malay subjects. PFAS were positively associated with a number of lipid species from lysophospholipid, ceramide and triacylglycerol lipid classes. Phosphatidylinositol, acylcarnitine and sphingosine-1-phosphate were negatively associated with PFAS. Association studies revealed both shared and distinct relationship of PFAS with plasma lipids. Conclusions: We demonstrate that the circulating levels of PFAS vary with age, ethnicity and sex within a multi-ethnic Asian population with potential implications in future biomonitoring and mitigation. Our comprehensive lipidomics methodology and association studies enabled us to characterize the relationship of circulating PFAS and lipidomic profiles. These results will help in better understanding of the molecular basis of PFAS exposure on human health outcomes. [ABSTRACT FROM AUTHOR]

Bis(monoacylglycero)phosphate (BMP) is an abundant lysosomal phospholipid required for degradation of lipids, particularly gangliosides. Alterations in BMP levels are associated with neurodegenerative diseases. Unlike typical glycerophospholipids, lysosomal BMP has two chiral glycerol carbons in the S (rather than the R) stereo-conformation, protecting it from lysosomal degradation. How this unusual and yet crucial S , S- stereochemistry is achieved is unknown. Here, we report that phospholipases D3 and D4 (PLD3 and PLD4) synthesize lysosomal S , S- BMP, with either enzyme catalyzing the critical glycerol stereo-inversion reaction in vitro. Deletion of PLD3 or PLD4 markedly reduced BMP levels in cells or in murine tissues where either enzyme is highly expressed (brain for PLD3; spleen for PLD4), leading to gangliosidosis and lysosomal abnormalities. PLD3 mutants associated with neurodegenerative diseases, including risk of Alzheimer's disease, diminished PLD3 catalytic activity. We conclude that PLD3/4 enzymes synthesize lysosomal S , S- BMP, a crucial lipid for maintaining brain health. [Display omitted] • Lysosomal S , S -BMP is stable, and its synthesis requires stereo-inversion of an R -glycerol • Purified PLD3 and PLD4 enzymes catalyze the synthesis of S , S- BMP in vitro • Cells or murine tissues lacking PLD3 or PLD4 have reduced BMP and accumulate gangliosides • Mutations in PLD3 implicated in neurodegeneration impair BMP synthesis activity Bis(monoacylglycero)phosphate (BMP) is an unusual phospholipid of lysosomes that is required for degradation of numerous lipids. Singh et al. discover that lysosomal S , S -BMP is synthesized by phospholipases D3 and D4 and that these enzymes linked to neurodegeneration are required for degradation of ganglioside lipids. [ABSTRACT FROM AUTHOR]

Primary liver cancer (PLC), which includes hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), remains a leading cause of cancer-related death worldwide. Chronic liver diseases, such as hepatitis B and C infections and metabolic dysfunction-associated steatotic liver disease (MASLD), are key risk factors for PLC. Metabolic reprogramming, a defining feature of cancer, enables liver cancer cells to adapt to the demands of rapid proliferation and the challenging tumor microenvironment (TME). This manuscript examines the pivotal role of metabolic reprogramming in PLC, with an emphasis on the alterations in glucose, lipid, and amino acid metabolism that drive tumor progression. The Warburg effect, marked by increased glycolysis, facilitates rapid energy production and biosynthesis of cellular components in HCC. Changes in lipid metabolism, including elevated de novo fatty acid synthesis and lipid oxidation, support membrane formation and energy storage essential for cancer cell survival. Amino acid metabolism, particularly glutamine utilization, supplies critical carbon and nitrogen for nucleotide synthesis and maintains redox homeostasis. These metabolic adaptations not only enhance tumor growth and invasion but also reshape the TME, promoting immune escape. Targeting these metabolic pathways presents promising therapeutic opportunities for PLC. This review underscores the interaction between metabolic reprogramming and tumor immunity, suggesting potential metabolic targets for innovative therapeutic strategies. A comprehensive understanding of PLC's intricate metabolic landscape may lead to more effective treatments and better patient outcomes. Integrating metabolomics, genomics, and proteomics in future research will be vital for identifying precise therapeutic targets and advancing personalized therapies for liver cancer. [ABSTRACT FROM AUTHOR]

The intramuscular oleic‐to‐stearic fatty acid ratio (C18:1n‐9/C18:0) is an important indicator of the biosynthesis and desaturation of fatty acids in muscle. By using an RNA‐Seq approach in muscle samples from 32 BC1_DU (25% Iberian and 75% Duroc) pigs with divergent values (high: H and low: L) of C18:1n‐9/C18:0 fatty acids ratio, a total of 81 differentially expressed genes (DEGs) were identified. Functional analyses of DEGs indicate that mainly peroxisome proliferator‐activated receptor signaling pathway (associated genes: PPARG, SCD, PLIN1, and FABP3) was overrepresented. Notably, SCD is directly involved in the conversion of C18:0 to C18:1n‐9, and PPARG is a transcription factor regulating lipid metabolism genes, including SCD. However, other DEGs (e.g., ACADVL, FADS3, EPHB2, HGFAC, NGFR, NR0B2, MDH1, MMAA, PPP1R1B, SFRP5, RAB30, and TRARG1) are plausible candidate genes to explain the phenotypic differences of the C18:1n‐9/C18:0 ratio. Interestingly, seven genetic variants within the SCD (including the well‐known AY487830:g.2228T>C SNP and other novel genotyped polymorphisms) are associated with two haplotypes. Although the haplotypes are segregating at different frequencies in the H and L groups, they do not fully explain the desaturation ratios or the SCD expression levels. A more complex model, including polyunsaturated fatty acids such as C18:2n‐6, C20:4n‐6, and C18:3n‐3, is suggested to explain the regulation of the C18:1n‐9/C18:0 desaturation ratio in porcine muscle. [ABSTRACT FROM AUTHOR]

Obesity and its associated inflammatory state pose a significant health burden. Anthocyanins, bioactive compounds found in fruits and vegetables, have garnered interest in their potential to attenuate these conditions. Understanding the dose‐dependent response of anthocyanins is essential for optimizing their therapeutic potential in preventing and managing obesity. This comprehensive review explores the current knowledge on the dose‐dependent effects of anthocyanins on obesity in both human and animal models, analyzing the structure and mechanism of absorption of these compounds. The article also highlights the diverse mechanisms underlying anthocyanin action, the symbiosis between anthocyanins and gut microbiota impacting metabolite production, influencing diverse health outcomes, modulating cytokines, and activating anti‐inflammatory pathways. Additionally, their impact on energy metabolism and lipid regulation is discussed, highlighting potential contributions to weight management through AMPK and PPARγ pathways. Despite promising results, dose‐dependent effects are fundamental considerations, with some studies indicating less favorable outcomes at higher doses. Future research should focus on optimizing dosages, accounting for individual responses, and translating findings into effective clinical applications for obesity management. [ABSTRACT FROM AUTHOR]

Background: Previous studies suggest that septic patients often have elevated triglyceride levels due to various factors, and higher levels may indicate a poorer prognosis. However, few studies have investigated whether lower triglycerides are associated with a better prognosis. Methods: The Medical Information Mart for Intensive Care IV (MIMIC-IV) database provided all the data. To assess the association between triglycerides and prognosis, we used logistic regression analysis (LR), least absolute shrinkage and selection operator (LASSO) and Cox proportional hazards models. Results: Inclusion criteria were met by a total of 804 patients with a mean triglyceride of 103 mg/dL. We found that patients had a higher risk of 30-day ICU mortality when triglycerides were in the second quartile (74–103 mg/dL). Interestingly, this group of patients seems to benefit more from the use of atorvastatin. Conclusion: Our study showed that septic patients with triglyceride levels in the second quartile (74–103 mg/dL) have a higher 30-day ICU mortality rate compared to those with triglyceride levels in other quartiles. [ABSTRACT FROM AUTHOR]

Background: To determine whether obesity and markers of lipid metabolism are associated with radiological hand osteoarthritis (OA) in the Halland County Osteoarthritis (HALLOA) cohort. Methods: In this cross-sectional study, we included 231 participants aged 30–65 from the HALLOA cohort, which began in 2017 and is ongoing. Hand OA was defined as ≥ 2 joint groups (distal interphalangeal, proximal interphalangeal, and carpometacarpal I) with Kellgren-Lawrence grade ≥ 2. The severity of hand OA was classified in terms of the number of affected joint groups (moderate hand OA 2–4 joint groups, severe hand OA 5–6 joint groups). Metabolic profile, including body mass index (BMI), bioimpedance, waist circumference, blood pressure, serum leptin, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides, were obtained. Multicollinearity was assessed with Pearson's correlation and associations with logistic regression analyses adjusting for age, HDL-cholesterol, and central obesity. Results: Two-thirds of the participants were women, and 91 (39%) had hand OA. We found a relationship between LDL-cholesterol and prevalent hand OA in women with an odds ratio of 1.7 (95% CI 1.1–2.6) and an association between LDL-cholesterol and severity of hand OA in women; odds ratio for no hand OA vs. moderate hand OA was 1.6 (95% CI 1.0-2.4) and for no hand OA vs. severe hand OA 2.5 (95% CI 1.2–4.9). There were no significant relationships between hand OA and obesity or serum leptin levels. Conclusion: Circulating LDL-cholesterol levels were associated with the prevalence and severity of hand OA in women but not men. Trial registration: ClinicalTrials. Gov (NCT04928170), Date of registration: 2017-12-20. [ABSTRACT FROM AUTHOR]

ABSTRACT The increase in global climate variability has increased the frequency and severity of floods, profoundly affecting agricultural production and food security worldwide. Autophagy is an intracellular catabolic pathway that is dispensable for plant responses to submergence. However, the physiological role of autophagy in plant response to submergence remains unclear. In this study, a multi‐omics approach was applied by combining transcriptomics, proteomics, and lipidomics to characterize molecular changes in the Arabidopsis autophagy‐defective mutant (atg5‐1) responding to submergence. Our results revealed that submergence resulted in remarkable changes in the transcriptome, proteome, and lipidome of Arabidopsis. Under submerged conditions, the levels of chloroplastidic lipids, including monogalactosyldiacylglycerol (MGDG), digalactosyldiacylglycerol (DGDG), and phosphatidylglycerol (PG), were lower in atg5‐1 than in wild‐type, suggesting that autophagy may affect photosynthesis by regulating lipid metabolism. Consistently, photosynthesis‐related proteins and photosynthetic efficiency decreased in atg5‐1 under submergence conditions. Phenotypic analysis revealed that inhibition of photosynthesis resulted in a decreased tolerance to submergence. Compared to wild‐type plants, atg5‐1 plants showed a significant decrease in starch content after submergence. Collectively, our findings reveal a novel role for autophagy in plant response to submergence via the regulation of underwater photosynthesis and starch content. [ABSTRACT FROM AUTHOR]

This trial was conducted to assess the effects of different levels of dietary fish oil on growth performance, hepatic health, nonspecific immune responses, and intestinal microbial community of Amur grayling (Thymallus grubii). Five isonitrogenous diets containing 60 (6FO), 90 (9FO), 120 (12FO), 150 (15FO), and 180 g/kg (18FO) fish oil were fed to triplicate groups of 60 fish per tank for 8 weeks, respectively. The results revealed that specific growth rate (SGR) and weight gain (WG) of fish in the 15FO group were significantly greater than those in the 6FO group (p < 0.05). Somatic indices and whole‐body lipid levels were positively correlated with increases in dietary fish oil levels. Trypsin and lipase activities in 15FO and 18FO groups were significantly higher than those in the 6FO and 9FO groups (p < 0.05). The activities of intestinal catalase (CAT) and liver superoxide dismutase (SOD), CAT, lysozyme (LZM), alkaline phosphatase (AKP), and acid phosphatase (ACP) improved significantly as the dietary lipid content increased to 185.3 g/kg and decreased thereafter (p < 0.05). The lipid metabolism‐related genes peroxisome proliferator‐activated receptor gamma (PPARγ) and carnitine palmitoyltransferase 1A (CPT1A) were significantly downregulated and upregulated (p < 0.05), respectively, in the 15FO group. Immune‐related genes in the liver and intestine, such as interleukin (IL‐8), were significantly upregulated in the 15FO group (p < 0.05). The liver sections from 18FO group presented more numerous and larger lipid vacuoles. Both low‐ (6FO) and high‐lipid (18FO) diets reduced the relative abundance of intestinal Lactococcus. The relative abundances of intestinal Staphylococcus and Bacillus (mainly Bacillus anthracis) increased in the low‐lipid diet group and that of Pedobacter increased in the high‐lipid diet group. Second‐order polynomial analysis of WG and the feed conversion ratio (FCR) for varying levels of dietary lipid revealed that a range of 194.76–198.90 g/kg dietary lipid was optimal for the growth and health of Amur grayling. [ABSTRACT FROM AUTHOR]

Background: At present, fat transplantation is widely used in the plastic surgery industry, but the long-term preservation rate of transplanted fat decreases because of complications such as oil cysts due to the inability in macrophages to metabolize absorption. In cell-assisted lipotransfer technology, adipose-derived stem cells (ASCs) can influence the inflammatory response of grafts through the immunoregulation in macrophages, and the lipid metabolism in macrophages plays an important role in this process. Therefore, we hypothesized ASCs could improve the retention rate of fat grafts by regulating the progress of lipid metabolism in macrophages. Methods: We established fat transplantation and ASC-assisted fat transplantation model in C57BL/6 mice in vivo, and bone marrow-derived macrophages cocultured with apoptotic adipocytes were treated with or without ASCs in vitro. Graft retention, tissue structure, fibrosis, macrophage phenotype transformation, lipid deposition, mitochondrial morphology, oxygen consumption rate (OCR), fatty acid β-oxidation (FAO) level, and ATP production were assessed. Additionally, fat transplantation and ASC-assisted fat transplantation model was treated with etomoxir which inhibits mitochondrial FAO. Macrophages pretreated with etomoxir were co-cultured with apoptotic adipocytes and treated with or without ASCs. The method aboved was used for detection and verification. Results: In vivo, ASC-assisted fat transplantation improved macrophage mitochondrial expression and FAO level, promoted the early transformation of M2 macrophages, reduced the long-term lipid deposition of macrophages, and improved the retention rate of fat grafts. In vitro, ASCs up-regulated the level of mitochondrial FAO, OCR and ATP production in macrophages, reduced lipid deposition of macrophages and promoted M2 macrophages polarization by paracine function. The ability of ASCs in group pretreated with etomoxir to reduce the foaming of macrophages, promote the transformation to M2 macrophages, and improve the retention rate of fat transplantation was weakened. Conclusions: ASCs increased the retention rate of transplanted fat by upregulating mitochondrial FAO to promote M2 polaration in macrophages. In addition, ASCs up-regulate mitochondrial FAO by paracrine effect to reduce foam cells formation and promote M2 transformation in macrophages in vitro. [ABSTRACT FROM AUTHOR]

ABSTRACT To investigate the synergistic effect of astaxanthin and curcumin on ovarian function in polycystic ovary syndrome (PCOS) mice and to elucidate the underlying mechanisms, fifty 4‐week‐old female mice were randomly divided into five groups: (i) normal control group; (ii) PCOS model group; (iii) PCOS + astaxanthin group; (iv) PCOS + curcumin group; and (v) PCOS + astaxanthin–curcumin. Throughout the study, various parameters were meticulously evaluated, including serum levels of key reproductive hormones (testosterone (T), estradiol (E2), follicle‐stimulating hormone (FSH), luteinizing hormone (LH), and anti‐Müllerian hormone (AMH)), as well as monitoring alterations in the estrous cycle, follicle development, and ovulation rates. Additionally, markers of oxidative stress and inflammation were measured. Findings revealed that PCOS mice exhibited disordered estrous cycle, polycystic ovarian morphologies, abnormal serum reproductive hormones and lipid metabolism, heightened oxidative stress, and augmented inflammatory responses. Notably, upon administration of the combined astaxanthin and curcumin, PCOS mice exhibited significant improvements in their estrous cyclicity and ovarian histology. The treatment led to a significant reduction in serum total cholesterol (TC) levels and normalization of T, E2, FSH, LH, and AMH levels. Moreover, there was a marked decrease in the levels of serum reactive oxygen species (ROS) and malondialdehyde (MDA), indicating attenuation of oxidative stress. Concurrently, the activity of the antioxidant enzyme catalase (CAT) significantly increased, while proinflammatory cytokines interferon‐γ (IFN‐γ) and interleukin‐6 (IL‐6) in the ovarian tissue were notably decreased. The combined treatment also resulted in a substantial increase in the number of ova and a significant decline in the rate of abnormal ova, with these therapeutic effects proving more effective compared to either astaxanthin or curcumin alone. In conclusion, the co‐administration of astaxanthin and curcumin demonstrated a remarkable effect in improving abnormal lipid metabolism and restoring reproductive endocrine functions in PCOS mice. Furthermore, it effectively mitigated systemic and local oxidative stress and chronic inflammatory injury, thereby promoting follicular growth and enhancing ovulatory function in the context of PCOS. [ABSTRACT FROM AUTHOR]

ABSTRACT The benefits of plant essential oils (EO) on the health of animals have been frequently reported, but their alteration of lipid metabolism in obese pigs has yet to be explored. This study aimed to assess the impact of EO blends (oregano, cinnamon and lemon oils) on growth performance, meat physicochemical parameters, intestinal health and lipid metabolism in the small intestine of weaned Bamei (a kind of obese‐type pig) piglets. One hundred and forty‐four male 60‐day‐old weaned Bamei piglets were randomly assigned to three groups of six replicates each: CON (basal diet), T1 (basal diet + 250 mg/kg EO), and T2 (basal diet + 500 mg/kg EO) over 28 days. The results showed that T1 trended to improve the average daily gain and feed intake to body gain ratio (p < 0.1), reduced water loss (p < 0.05), and increased the redness of meat (p < 0.05) compared to the CON. In addition, a significant change in the proportion of C17:0 and C20:1 was observed in the meat of T1 (p < 0.05). Improved intestinal health was evidenced by the reduced crypt depth, improved villi‐to‐crypt length ratio, and better superoxide dismutase activity in T1 (p < 0.05). Further study on intestinal lipid metabolism showed that duodenal lipase activity and the mRNA expression levels of lipid transport‐related genes in the jejunum (FABPs, APOA1, APOB and ACSL3) were significantly reduced, alongside diminished serum lipid metabolites (Total protein and triglyceride) in the groups fed with EO (p < 0.05). In short, EO supplementation especially at 250 mg/kg improved intestinal health and inhibited lipid metabolism, which had a positive effect on the overall performance of Bamei piglets. This new evidence contributes to understanding the early regulatory role of EO in obese pigs and their potential to alleviate adolescent obesity. [ABSTRACT FROM AUTHOR]

The initial stage of alcoholic liver disease (ALD) is hepatic steatosis. Recent studies have highlighted a possible role for Apoptosis-stimulating protein 2 of p53 (ASPP2) in regulating hepatic lipid metabolism in nonalcoholic fatty liver (NAFLD). However, whether ASPP2 regulates alcohol-induced lipid accumulation and its mechanisms remain unclear. To explore that, we establish an alcoholic liver injury model in vivo and in vitro. The clinical specimens were collected from liver tissues of patients with alcoholic liver disease. Lipid metabolism was detected by HE staining, oil red O staining and qPCR; and ASPP2-peroxisome proliferator-activated receptor γ (PPARγ) signaling pathways were detected by western blot and immunohistochemical staining. We found that both ASPP2 and PPARγ expression increased in patients and mouse models with ALD. We also discovered the reduction of ASPP2 significantly inhibited the expression of PPARγ and alleviated alcohol-induced hepatic lipid accumulation and liver injury in vivo and in vitro. Mechanistically, the PPARγ agonist reversed the protective effect of ASPP2 downregulation on hepatic steatosis and liver injury, while the opposite results were observed using PPARγ inhibitor. In conclusion, ASPP2 exacerbates ethanol-induced lipid accumulation and hepatic injury by upregulating the PPARγ signaling pathway, thus promoting the occurrence and development of ALD. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a multifaceted autoimmune disease affecting various body organs and systems. The diagnosis of SLE and its complications is based on evident clinical symptoms, serological marker levels, and pathological findings. Some serological markers have a low sensitivity and specificity, and biopsy procedures are invasive in nature. Hence, metabolomics has emerged as a valuable tool for SLE screening and categorization. Its application has contributed significantly to identifying SLE pathogenesis, improving clinical diagnosis, and developing treatment approaches. This review provides an overview of the utilization of metabolomics in the study of SLE, focusing on advancements in understanding the disease's pathogenesis, aiding in diagnosis, and monitoring treatment efficacy. [ABSTRACT FROM AUTHOR]

The low‐density lipoprotein receptor (LDLr) is the first member of a closely related transmembrane protein family. It is known for its involvement in various physiological processes, mainly in the regulation of lipid metabolism, especially in the brains of mammals and zebrafish. In zebrafish, two ldlr genes (ldlra and b) have been identified and their distribution in the brain is not well documented. Recently, the roles of ldlr and its inhibitor pcsk9 in regenerative process after telencephalic brain injury have been discussed. In this study, we explored the expression patterns of these genes during zebrafish development. We found that ldlra expression was detected at the end of the pharyngula period (48 hpf) and increased during the larval stage. Conversely, ldlrb expression was observed from zygotic to larval stages. Using techniques like in situ hybridization and taking advantage of transgenic fish, we demonstrated the widespread distribution of ldlra, ldlrb and pcsk9 in the brain of adult zebrafish. Specifically, these genes were expressed in neurons and neural stem cells and also at lower levels in endothelial cells. As expected, intraperitoneal injection of fluorescent‐labelled LDLs resulted in their uptake by cerebral endothelial cells in a homeostatic context, whereas they diffused within the brain parenchyma after telencephalic injury. However, after intracerebroventricular injections into animals, LDL particles were not taken up by neural stem cells. In conclusion, our results provide additional evidence for LDLr expression in the brain of adult zebrafish. These results raise the question of the role of LDLr in the cholesterol/lipid imbalance in cerebral complications. [ABSTRACT FROM AUTHOR]

Background: The relationship between hepatocellular carcinoma (HCC) metastasis and cancer metabolism reprogramming is becoming increasingly evident. Ubiquitin-specific protease 11 (USP11), a member of the deubiquitinating enzyme family, has been linked to various cancer-related processes. While USP11 is known to promote HCC metastasis and proliferation, the precise mechanisms, especially those related to cancer metabolism, remain unclear. Methods: Through mass spectrometry, co-immunoprecipitation, immunofluorescence, and ubiquitination assays, we identified USP11 as the key deubiquitinase for SREBF1.Lipogenesis was evaluated using Oil Red O and Nile Red staining, along with the detection of triglycerides and cholesterol. To assess HCC cell proliferation, migration, and invasion in vitro, Transwell assays, EDU, colony formation, and CCK-8 were conducted. Xenograft models in nude mice were developed to verify the role of the USP11/SREBF1 axis in lipogenesis and tumor growth in vivo. Results: USP11 directly interacts with SREBF1, and its silencing leads to the disruption of SREBF1 stabilization through K48-linked deubiquitination and degradation. Importantly, the truncated mutant USP11 (503–938 aa) interacts with the truncated mutant SREBF1 (569–1147aa), with K1151 playing a crucial role in this interaction. Higher levels of USP11 enhance lipogenesis, proliferation, and metastasis in HCC cells. Importantly, the knockdown of SREBF1 weakened the effects of USP11 in enhancing lipogenesis and tumorigenesis. Futhermore, the elevated expression of USP11 and SREBF1 in HCC tissue serves as an indicator of poor prognosis in HCC patients. Conclusions: In summary, our study reveals that USP11 promotes HCC proliferation and metastasis through SREBF1-induced lipogenesis. These findings provide a foundation for novel therapies targeting lipid metabolism in HCC. [ABSTRACT FROM AUTHOR]

Polyamines are critical cellular components that regulate a variety of processes, including translation, cell cycling, and nucleic acid metabolism. The polyamines, putrescine, spermidine, and spermine, are found abundantly within cells and are positively-charged at physiological pH. Polyamine metabolism is connected to distinct other metabolic pathways, including nucleotide and amino acid metabolism. However, the breadth of the effect of polyamines on cellular metabolism remains to be fully understood. We recently demonstrated a role for polyamines in cholesterol metabolism, and following these studies, we measured the impact of polyamines on global lipid metabolism. We find that lipid droplets increase in number and size with polyamine depletion. We further demonstrate that lipid anabolism is markedly decreased, and lipid accumulation is due to reduced mitochondrial fatty acid oxidation. In fact, mitochondrial structure and function are largely ablated with polyamine depletion. To compensate, cells depleted of polyamines switch from aerobic respiration to glycolysis in a polyamine depletion-mediated Warburg-like effect. Finally, we show that inhibitors of lipid metabolism are broadly antiviral, suggesting that polyamines and lipids are promising antiviral targets. Together, these data demonstrate a novel role for polyamines in mitochondrial function, lipid metabolism, and cellular energetics. Author summary: Cells and viruses rely on metabolic circuits to survive and replicate. The small metabolites called polyamines support cellular homeostasis by supporting mitochondrial function. Without polyamines, lipids accumulate in cells because they are not catabolized by fatty acid oxidation. Cells depleted of polyamines switch from aerobic respiration to glycolysis for energy production, similar to cancer cells in hypoxic environments. We also show that varied viruses use lipids to replicate, and targeting lipids with small molecule inhibitors can reduce virus replication. Overall, our work makes a new connection between polyamines and lipid metabolism and highlights potential pathways to target for antiviral therapies. [ABSTRACT FROM AUTHOR]

Previous studies have reported that a potential association between exposure to outdoor light at night (LAN) and diseases. However, there is no evidence regarding the impacts of outdoor LAN exposure on lipid metabolism in humans. This study aims to evaluate the associations between outdoor LAN exposure and the prevalence of dyslipidemia, using a nationwide sample of 10,894 adults aged ≥ 45 years from 150 investigated sites across China in 2011–2012. Outdoor LAN exposure was assessed by using satellite imaging data. The prevalence ratio (PR) was calculated. The present study found that a per-quintile LAN exposure was positively associated with the prevalence of high LDL-cholesterol (PR = 1.10, 95% CI = 1.04–1.16), high triglyceride (PR = 1.07, 95% CI = 1.03–1.12), low HDL-cholesterol (PR = 1.11, 95% CI = 1.08–1.16), and dyslipidemia (PR = 1.06, 95% CI = 1.03–1.09). The fifth quintile of LAN exposure was associated with a significantly increased prevalence of dyslipidemia (PR = 1.20, 95% CI = 1.07–1.35) compared with the first quintile of exposure. Long-term exposure to outdoor LAN was positively associated with dyslipidemia prevalence. Public policies aimed at reducing light pollution at night, guided by the spatial distribution patterns, could lessen the adverse effects. [ABSTRACT FROM AUTHOR]

Background: Both lipid metabolism and cyclic RNAs (circRNAs) have been found to be involved in pancreatic adenocarcinoma (PAAD) progression, but the relationship between lipid metabolism and circRNAs remains unclear. Methods: The expression levels of miR-223-3p, circ_0124346, and acyl-CoA synthetase long chain family member 3 (ACSL3) were determined through qRT-PCR and Western blot analysis. Cell proliferation was evaluated using the CCK-8 and EdU incorporation assays. Cholesterol (CH) and triglyceride (TG) levels were quantified using relevant kits. The relationships between miR-223-3p and circ_0124346 or ACSL3 mRNA were examined by bioinformatics analysis, luciferase reporter, RNA-RNA pull-down, and RIP assays. Results: We observed a significant elevation in circ_0124346 expression in both pancreatic adenocarcinoma (PAAD) tissues and cell lines, and its expression level was shown to be correlated with tumor size. Circ_0124346 stimulated cell proliferation and facilitated lipid synthesis in PAAD cells. Additionally, we found that circ_0124346 functioned as a sponge for miR-223-3p, preventing miR-223-3p's binding to the 3'-UTR of ACSL3 mRNA, which subsequently led to an elevation in ACSL3 expression and promoted lipid synthesis. Accordingly, circ_0124346 knockdown resulted in a significant decrease in lipid synthesis and cell proliferation in PAAD cells, with partial reversal of these effects achieved via inhibiting miR-223-3p or overexpressing ACSL3. Conclusion: Our study demonstrated that circ_0124346 regulates lipid metabolism in PAAD cells via the miR-223-3p/ACSL3 axis, suggesting that targeting circ_0124346 may serve as a potential strategy for treating PAAD and assisting in its diagnosis. [ABSTRACT FROM AUTHOR]

Lipid metabolism reprogramming has emerged as a hallmark of malignant tumors. Lipids represent a complex group of biomolecules that not only compose the essential components of biological membranes and act as an energy source, but also function as messengers to integrate various signaling pathways. In tumor cells, de novo lipogenesis plays a crucial role in acquiring lipids to meet the demands of rapid growth. Increasing evidence has suggested that dysregulated lipid metabolism serves as a driver of cancer progression. Posttranslational modifications (PTMs), which occurs in most eukaryotic proteins throughout their lifetimes, affect the activity, abundance, function, localization, and interactions of target proteins. PTMs of crucial molecules are potential intervention sites and are emerging as promising strategies for the cancer treatment. However, there is limited information available regarding the PTMs that occur in cancer lipid metabolism and the potential treatment strategies associated with these PTMs. Herein, we summarize current knowledge of the roles and regulatory mechanisms of PTMs in lipid metabolism. Understanding the roles of PTMs in lipid metabolism in cancer could provide valuable insights into tumorigenesis and progression. Moreover, targeting PTMs in cancer lipid metabolism might represent a promising novel therapeutic strategy. [ABSTRACT FROM AUTHOR]

Simple Summary: The Krškopolje pig has a reputation for being more resilient and having a lower protein requirement compared to modern breeds, which is important for sustainable agriculture. However, this difference needs to be proven by comparing the genotypes under the same conditions. The present study compares this indigenous Slovenian breed with modern hybrid pigs, investigating the effects of reduced dietary protein intake on growth and meat quality. Our research showed that dietary protein reduction in modern pigs led to a slight decrease in performance but not in Krškopolje pigs, confirming its lower protein requirement and better adaptability. Overall, the modern pigs grew faster and deposited more muscle, while the Krškopolje pigs deposited more fat. Their fat was also more saturated. The meat from Krškopolje pigs showed a better aptitude for processing into high-quality meat products. The results obtained can help farmers in rearing Krškopolje pigs more efficiently and thus preserve the breed and offer high-quality meat products. This study compared the performance, meat quality and adipose tissue characteristics of Krškopolje pigs and modern hybrid pigs under identical rearing conditions, besides examining the effects of dietary protein reduction in both genotypes. A total of 29 pigs (14 Krškopolje and 15 hybrids) were assigned to litter into two dietary groups (high and low protein). The low-protein diet for hybrid pigs corresponded to the high-protein diet for Krškopolje pigs. All diets were iso-energetic. Dietary protein reduction decreased growth rate and muscle development in modern hybrids but had no significant impact on performance, quality or metabolic traits in Krškopolje pigs. Genotype differences revealed that Krškopolje pigs had lower growth rates, less lean and more fat deposition, as reflected in thicker subcutaneous and higher intramuscular fat compared to modern hybrids. Krškopolje pigs also exhibited higher myoglobin concentration and fatty acid saturation. Lipogenic enzyme activity and histo-morphological traits behaved in a tissue-specific manner but still indicated a greater lipogenic potential in Krškopolje pigs. This study provides valuable insights into breed-specific responses to dietary changes and highlights the unique characteristics of Krškopolje pigs. [ABSTRACT FROM AUTHOR]

Simple Summary: Polyunsaturated fatty acids (PUFAs), especially those obtained from microalgae, are an efficient and sustainable strategy to enrich ruminant products with biofunctional molecules. However, the high dietary inclusion needed to substantially affect product quality can also bring negative effects on lipid metabolism. The dietary forage-to-concentrate ratio (F:C) is also a lever to drive metabolic functions, including lipid metabolism, with the advantage of its easy manipulation. To address this hypothesis, we conducted an experiment assessing the interaction of two inclusion levels of Schizochytrium spp. (20 or 40 g/day), a microalga rich in PUFA, and two F:C ratios (60/40 or 40/60) on regulating gene networks involved in lipid metabolism in goats' tail fat. Results showed a decreasing gene expression under the effect of high microalgae levels or the high-grain diet. However, when the diet was based on forages, the negative effect of high microalgae levels on lipogenic gene expression was more attenuated. Long-chain polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA) have been shown to be effective in enhancing the quality of ruminant products, including meat and milk. However, under these dietary conditions, the de novo lipogenesis could be influenced, too. On the other hand, even if the forage-to-concentrate ratio (F:C) is also a key factor affecting lipid metabolism in small ruminants, there is scarce information about its interaction with dietary PUFA. This study investigates the potential of the F:C ratio as a lever to manipulate lipid metabolism in dairy goats under high dietary PUFA supplementation. For this purpose, twenty-two crossbred dairy goats [Alpine × Local (Greek) breeds] (BW = 50.6 ± 6.1 kg) at early lactation (70 ± 10 days in milk) during the age of 3–4 years old, were separated into two homogeneous subgroups (n = 11). In the first phase, each goat was fed 20 g Schizochytrium spp./day followed by either a high-forage (20 HF) or a high-grain (20 HG) diet, while in the second phase, each goat was fed 40 g Schizochytrium spp./day followed once again either a high-forage (40 HF) or a high-grain (40 HG) diet. The F:C ratio of a high-forage and high-grain diet was 60:40 and 40:60, respectively. Tail fat tissue samples were collected by biopsy on the 42nd day of each experimental phase (last day). Significant decreases (p < 0.05) in the gene expression of ACACA, CBR2, COX4I1, ELOVL5, ELOVL7, LEP, and SCD were presented in goats fed 40 g compared to those fed 20 g Schizochytrium spp., while the gene expression of ACACA, AGPAT2, AGPAT3, ELOVL5, ELOVL6, EPHX2, FASN, and SCD was decreased in high grain compared to high-forage diets. This study also indicated that with the aim to enrich goat products with PUFA by increasing their levels in the diet, lipid metabolism is negatively affected. However, a diet with higher forage inclusion can partially attenuate this condition. [ABSTRACT FROM AUTHOR]

Simple Summary: In this study, six SNPs (UTR-(-127) C>A, UTR-(-105) T>A, UTR-(-87) G>A, I1-763 G>T, E2-77 G>A, E2-127 G>T) were detected in the IFI27 gene in a Chinese Holstein cow population. In addition, association analysis of the polymorphism of IFI27 and milk quality traits showed that the AG and GG genotypes of E2-77 G>A, and the GG and the TT genotypes of E2-127 G>T were connected to milk fat. Haplotype frequency analysis showed that individuals with an H5H6 genotype produced higher milk fat content than these with an H5H5 haplotype combination. Moreover, overexpression of the IFI27 gene in bovine mammary epithelial cells caused a significant increase in triglycerides content and a decrease in cholesterol and nonestesterified fatty acid content, while interference with IFI27 expression produced opposing changes. These results provide reference for the selection of milk fat traits in dairy cattle breeding and lay the foundation for further research of IFI27 gene function in milk fat metabolism. Milk fat is an important indicator for evaluating milk quality and a symbol of the core competitiveness of the dairy industry. It can be improved through genetic and feed management factors. Interferon alpha-inducible protein 27 (IFI27) was found to be differentially expressed when comparing the transcriptome in high- and low-fat bovine mammary epithelial cells (bMECs) in our previous research. Therefore, this study aimed to investigate whether the IFI27 gene had a regulatory effect on lipid metabolism.We detected six SNPs in the IFI27 gene (UTR-(-127) C>A, UTR-(-105) T>A, UTR-(-87) G>A, I1-763 G>T, E2-77 G>A, E2-127 G>T) in a Chinese Holstein cow population. Association analysis of the polymorphism of IFI27 and milk quality traits showed that the AG and GG genotype of E2-77 G>A, and the GG and TT genotypes of E2-127 G>T were connected to milk fat (p < 0.05). Haplotype frequency analysis showed that H5H5 was associated with lower milk fat content (p < 0.05), while milk from H5H6 animals had a higher fat content (p < 0.05). Subsequently, IFI27 overexpression vectors (PBI-CMV3-IFI27) and interference vectors (Pb7sk-GFP-shRNA) were constructed. Overexpression of the IFI27 gene in bMECs caused a significant increase in triglycerides (TGs) content (p < 0.05) and decreases in cholesterol (CHOL) and nonestesterified fatty acid (NEFA) content (p < 0.05), while interference with IFI27 expression produced opposing changes (p < 0.05). In summary, IFI27 E2-77 G>A and IFI27 E2-127 G>T may be useful as molecular markers in dairy cattle to measure milk fat, and the IFI27 gene may play an important role in milk lipid metabolism. [ABSTRACT FROM AUTHOR]

Simple Summary: With the improvement of living standards, people's requirements for meat quality are also growing. Reducing backfat thickness and inhibiting subcutaneous fat deposition is crucial for improving the quality of meat. Acorns are rich in nutrients and have antioxidant and hypoglycemic effects. The present study evaluated the role of acorns as a novel feed resource for pig production and found that an acorn diet had positive effects on lean meat rate, blood lipids and the inhibition of subcutaneous fat. The objective of the present research was the examination of how varying proportions of an acorn diet affects the deposition of subcutaneous fat and the composition of fatty acids (FAs) in Yuxi black pigs. Ninety pigs (with a balanced sex ratio and a similar weight 99.60 ± 2.32 kg) were stochastically assigned to the control group (CON) and the dietary acorn experimental groups (AEG). The CON was fed basal diets and the AEG1, AEG2, AEG3, and AEG4 groups were provided with dietary regimens comprising twenty, thirty, forty, and fifty per cent acorns, respectively. Each group consisted of six pigs, with three replicates. The breeding cycle was four months. The results demonstrated that, in comparison with the CON group, the lean meat rate was significantly increased in all test groups (p < 0.05), while in backfat thickness, loin eye area, carcass weight and slaughter rate was no significant difference (p > 0.05). The serum TC/HDL (total cholesterol divided by high-density lipoprotein-cholesterol) and TG/HDL (Triglyceride divided by high-density lipoprotein-cholesterol) levels in the AEG1 and AEG2 groups were significantly lower than the CON group (p < 0.05). There was no significant effect on the composition of FAs (p > 0.05). The number of fat cells in subcutaneous back fat and subcutaneous abdominal fat was significantly increased, and the area of fat cells was decreased (p < 0.05). Furthermore, the levels of ATGL and HSL expression in the subcutaneous back fat, as well as ACC, FAS, ATGL, PPARγ, and HSL expression in the subcutaneous abdominal fat, were significantly increased in the AEG2 group compared to the CON group (p < 0.05). Additionally, the expression of ACC, FAS, FABP4, PPARγ, C/EBPα, and FAS/HSL in the subcutaneous back fat, as well as FABP4, C/EBPα, and FAS/HSL in the subcutaneous abdominal fat, were significantly lower in the AEG2 group compared to the CON group (p < 0.05). In conclusion, it has been found that a 30% acorn diet can inhibit subcutaneous fat deposition and enhance the nutritional value of pork and the health of Yuxi black pigs. [ABSTRACT FROM AUTHOR]

Simple Summary: Sleep is a vital physiological process essential for maintaining mental and physical health. Insufficient sleep affects various physiological processes, including liver function and metabolism. In this study, we used a Tibetan sheep model for the first time to investigate the effects of sleep deprivation (SD) for 7 days (6 h/day) on liver function and circadian rhythms. We found that SD significantly disrupted the expression patterns of circadian rhythm genes in the liver. Gene enrichment analysis further indicated alterations in pathways related to lipid metabolism in the liver, suggesting that SD resets the expression of metabolic genes, causing liver damage by disrupting lipid metabolism. Sleep deprivation (SD) disrupts circadian rhythms; however, its effects on SD and the mechanisms involved require further investigation. Previous studies on SD were mainly conducted on rodents, such as mice, with few studies on its effects on the liver of large diurnal animals, such as sheep. In this study, we used a Tibetan sheep model for the first time to investigate the effects of SD on the liver by exposing Tibetan sheep (Ovis aries) to 7 days of SD (6 h/day) and performed transcriptome sequencing analysis on liver samples taken at 4 h intervals over 24 h. The results revealed that SD significantly altered the circadian expression of genes and their expression patterns in the liver of Tibetan sheep. Enrichment analysis of the circadian rhythm-altered genes revealed changes in the pathways related to lipid metabolism in the liver. Further evidence from serum markers and gene expression analyses using qualitative real-time polymerase chain reaction and Oil Red O and apoptosis staining indicated that SD leads to abnormal lipid metabolism in the liver, potentially causing liver damage. Therefore, our results suggest that SD disrupts the circadian rhythms of metabolism-related genes in the Tibetan sheep liver, thereby affecting metabolic homeostasis. [ABSTRACT FROM AUTHOR]