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Fatty liver syndrome (FLS) is a common metabolic disease in laying hens, causing reduced egg production and sudden death. Phyllanthus urinaria (PU), a traditional Asian herbal medicine, is known for its anti-inflammatory and hepatoprotective properties. This study investigated the hepatoprotective effects of water-extracted PU on FLS in both in vivo and in vitro chicken models. In oleic-acid (OA)-induced chicken hepatocytes, PU water extracts significantly reduced triglyceride accumulation and enhanced β-oxidation gene expression (CPT1α and PPARα). In palmitic-acid (PA)-induced hepatocytes, PU extracts curbed oxidative stress and decreased expression of the inflammation receptor TLR4. For the in vivo study, eight-week-old Lohmann layer pullets were divided into five groups: a control diet, a 2% FLS-inducing high cholesterol (HC) diet and HC diet with 0.5% PU, 1.0% PU or metformin (positive control) for six weeks. The HC diet significantly increased fatty scores, hepatic lipid accumulation, inflammation and oxidative stress. PU supplementation improved fatty liver scores, reduced hepatic lipid vacuole area, plasma triglyceride (TG) and serum thiobarbituric acid reactive substances (TBARS) levels, abdominal fat and hepatic inflammatory gene expression (TLR4, IL-1β, LITAF). In conclusion, PU improves FLS by reducing plasma TG and serum TBARS levels, body fats and inflammation while enhancing β-oxidation. PU shows potential as a dietary supplement and therapeutic agent for fatty liver diseases in humans and chickens.

ABSTRACT: High-laying ducks are often fed high-energy, nutritious feeds to maintain high productivity, which predisposes them to lipid metabolism disorders and the development of fatty liver syndrome (FLS), which seriously affects production performance and has a substantial economic impact on the poultry industry. Therefore, it is necessary to elucidate the mechanisms underlying the development of fatty liver syndrome. In this study, seven Shan Partridge ducks, each with fatty liver syndrome and normal laying ducks, were selected, and Hematoxylin Eosin staining (HE staining), Masson staining, and transcriptome sequencing were performed on liver tissue. In addition to exploring key genes and pathways using conventional analysis methods, we constructed the first Kyoto Encyclopedia of Genes and Genomes (KEGG) database-based predefined gene set containing 12,764 pathways and 16,836 genes and further performed gene set enrichment analysis (GSEA) on the liver transcriptome data. Finally, key nodes and biological processes were identified via the protein-protein interaction (PPI) network. The results showed that the liver in the FL group exhibited steatosis and fibrosis, and a total of 3,663 genes with upregulated expression versus 2,296 downregulated genes were screened by conventional analysis. GSEA analysis and PPI network analysis revealed that the liver in the FL group exhibited disruption of the mitochondrial electron transport chain, leading to decreased oxidative phosphorylation and the secretion of excessive proinflammatory factors amid the continuous accumulation of lipids. Under continuous chronic inflammation, cell cycle arrest triggers apoptosis, while fibrosis becomes more severe, and procarcinogenic genes are activated, leading to the continuous development and deterioration of the liver. In conclusion, the predefined gene set constructed in this study can be used for GSEA, and the identified hub genes provide useful reference data and a solid foundation for the study of the genetic regulatory mechanism of fatty liver syndrome in ducks.

[Objectives]This study aimed to investigate the effect of dietary bile acids(BA)supplementation on alleviating fatty liver syndrome(FLS)induced by corticosterone(CORT)in broilers, and the mechanism involving in this process. [Methods]One hundred and twenty 1-day-old AA male broilers were randomly divided into two groups and fed a basal diet or a BA containing diet respectively. BA were periodically added to the diet using the dose-escalation strategy including early, middle and late stages. At 28 days of age, twenty broilers were randomly selected from the basal diet group and divided into control group(CON)and corticosterone treatment group(CORT). Ten broilers fed BA were randomly picked up and set as corticosterone plus bile acids group(CORT+BA). The broilers were slaughtered at 40 days of age. The weight of organs and tissues was recorded. The serum and liver tissues were sampled for biochemical analysis and hepatic genes or proteins expression analysis. [Results]BA treatment significantly alleviated the deposition of abdominal fat and the decrease of leg muscle weight induced by CORT injection, and also increased leg muscle percentage(P<0.05). The results of biochemical analysis showed that CORT treatment significantly decreased serum high-density lipoprotein(HDLC)concentration, but increased serum non-esterified fatty acid(NEFA)level, while BA significantly increased the level of serum HDLC(P<0.05). The level of hepatic triglyceride(TG)was significantly increased by CORT(P<0.01)and the lipid droplets in liver were significantly enriched and vacuolated. However, these changes were markedly alleviated by BA treatment(P<0.05). Compared to the CON group, CORT significantly up-regulated the mRNA expression of stearoyl-CoA desaturase 1(scd1)and acetyl CoA carboxylase(acc)genes, and also significantly up-regulated the protein expression of ACC and fatty acid synthase(FASN)but down-regulated peroxisome proliferator activated receptor alpha(PPARα)protein expression in the liver(P<0.05). BA supplementation ameliorated the disorders of hepatic lipid metabolism caused by CORT and increased the mRNA expression of carnitine palmitoyl-transferase 1A(cpt1a)and decreased protein expression of fatty acid translocase(CD36)(P<0.05). [Conclusions]Dietary BA supplementation can significantly alleviate hepatic TG deposition induced by CORT through decreasing hepatic TG synthesis, promoting fatty acid decomposition, as well as inhibiting hepatic fatty acids uptake in broilers. [ABSTRACT FROM AUTHOR]

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Simple Summary: Fatty liver syndrome (FLS) in laying hens has brought serious economic losses to the poultry industry. Therefore, research on feed additives to alleviate FLS is necessary. This study investigated the effects of methyl sulfonyl methane (MSM) and selenium yeast (Se-Y) in the diet of laying hens on production performance, liver steatosis, and antioxidant index and explored the biological mechanisms of MSM and Se-Y to alleviate FLS via RNA-seq technology. The results provide a reference for the prevention and treatment of FLS in laying hens during the late peak laying period. The purpose of this study was to explore the effects of MSM and Se-Y on FLS in laying hens during the late peak laying period and the underlying biological mechanisms. Therefore 240 55-week-old Jing-fen No. 6 laying hens were randomly divided into five groups, with eight replicates in each group and six laying hens in each replicate. The hens were fed a basal diet (Control) and diets supplemented with 350 and 700 mg/kg MSM and 25 and 50 mg/kg Se-Y, respectively, for four weeks. The results showed that MSM and Se-Y had no significant effects on the performance of laying hens. With the increasing dosage of MSM and Se-Y, the symptoms of liver steatosis in laying hens were reduced, and MSM and Se-Y could significantly reduce the content of malondialdehyde (MDA) in serum and liver (p < 0.05) and increase the contents of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPX) in serum and liver (p < 0.05). The RNA-seq results showed that 700 mg/kg MSM significantly downregulated the expression levels of the ATP5I, ATP5G1, CYCS, and UQCRQ genes in the liver, and 50 mg/kg Se-Y significantly downregulated the expression levels of MAPK10, SRC, BMP2, and FGF9 genes in the liver. In conclusion, dietary supplementation with MSM and Se-Y can effectively reduce the FLS of laying hens in the late peak laying period and increase their antioxidant capacity. The underlying biological mechanism may be related to the downregulation of genes involved in liver oxidative phosphorylation and inflammation-related pathways. [ABSTRACT FROM AUTHOR]

Poultry oil is commonly used as a cost-effective energy source in poultry feed. However, when used at higher levels, raw poultry oil has been found to have adverse effects on the liver of birds. Unfortunately, many poultry farmers remain unaware of these harmful effects. The objective of this experiment was to investigate how poultry oil impacts liver health and contributes to fatty liver syndrome in layers. Using a completely randomized design, 120 Lohmann Single Comb (LSL-Lite) layers (25-week-old) were randomly assigned to 4 experimental groups, each of which had 30 birds. Increasing amounts of poultry oil (0, 1.5, 3.0 and 4.5%) were used in experimental diets. Hens were fed these experimental diets for 20 weeks. The results showed maximum liver fat percentage in 4.5% poultry oil in diet, severe liver congestion, degeneration and cell necrosis in caged layers. Plasma lipid profile (cholesterol, HDL, LDL, triglycerides) and liver enzymes (AST, ALT, ALP and LDH) were significantly (p<0.05) affected by poultry oil addition. Higher liver scores indicative of fatty liver syndrome was observed in layers receiving 4.5% poultry oil, while the control group showed the lowest incidence. This study indicated that poultry oil dietary addition at a higher level (4.5%) lead to an increased serum lipid profile and has a negative impact on liver health, ultimately causing fatty liver syndrome in caged layers. [ABSTRACT FROM AUTHOR]

High-laying ducks are often fed high-energy, nutritious feeds to maintain high productivity, which predisposes them to lipid metabolism disorders and the development of fatty liver syndrome (FLS), which seriously affects production performance and has a substantial economic impact on the poultry industry. Therefore, it is necessary to elucidate the mechanisms underlying the development of fatty liver syndrome. In this study, seven Shan Partridge ducks, each with fatty liver syndrome and normal laying ducks, were selected, and Hematoxylin Eosin staining (HE staining), Masson staining, and transcriptome sequencing were performed on liver tissue. In addition to exploring key genes and pathways using conventional analysis methods, we constructed the first Kyoto Encyclopedia of Genes and Genomes (KEGG) database-based predefined gene set containing 12,764 pathways and 16,836 genes and further performed gene set enrichment analysis (GSEA) on the liver transcriptome data. Finally, key nodes and biological processes were identified via the protein-protein interaction (PPI) network. The results showed that the liver in the FL group exhibited steatosis and fibrosis, and a total of 3,663 genes with upregulated expression versus 2,296 downregulated genes were screened by conventional analysis. GSEA analysis and PPI network analysis revealed that the liver in the FL group exhibited disruption of the mitochondrial electron transport chain, leading to decreased oxidative phosphorylation and the secretion of excessive proinflammatory factors amid the continuous accumulation of lipids. Under continuous chronic inflammation, cell cycle arrest triggers apoptosis, while fibrosis becomes more severe, and procarcinogenic genes are activated, leading to the continuous development and deterioration of the liver. In conclusion, the predefined gene set constructed in this study can be used for GSEA, and the identified hub genes provide useful reference data and a solid foundation for the study of the genetic regulatory mechanism of fatty liver syndrome in ducks. [ABSTRACT FROM AUTHOR]

Abstract Background Glucocorticoid receptor (GR) mediated corticosterone-induced fatty liver syndrome (FLS) in the chicken by transactivation of Fat mass and obesity associated gene (FTO), leading to demethylation of N6-methyladenosine (m6A) and post-transcriptional activation of lipogenic genes. Nutrition is considered the main cause of FLS in the modern poultry industry. Therefore, this study was aimed to investigate whether GR and m6A modification are involved in high-energy and low protein (HELP) diet-induced FLS in laying hens, and if true, what specific m6A sites of lipogenic genes are modified and how GR mediates m6A-dependent lipogenic gene activation in HELP diet-induced FLS in the chicken. Results Laying hens fed HELP diet exhibit excess (P

The purpose of this study was to explore the effects of MSM and Se-Y on FLS in laying hens during the late peak laying period and the underlying biological mechanisms. Therefore 240 55-week-old Jing-fen No. 6 laying hens were randomly divided into five groups, with eight replicates in each group and six laying hens in each replicate. The hens were fed a basal diet (Control) and diets supplemented with 350 and 700 mg/kg MSM and 25 and 50 mg/kg Se-Y, respectively, for four weeks. The results showed that MSM and Se-Y had no significant effects on the performance of laying hens. With the increasing dosage of MSM and Se-Y, the symptoms of liver steatosis in laying hens were reduced, and MSM and Se-Y could significantly reduce the content of malondialdehyde (MDA) in serum and liver (p < 0.05) and increase the contents of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPX) in serum and liver (p < 0.05). The RNA-seq results showed that 700 mg/kg MSM significantly downregulated the expression levels of the ATP5I, ATP5G1, CYCS, and UQCRQ genes in the liver, and 50 mg/kg Se-Y significantly downregulated the expression levels of MAPK10, SRC, BMP2, and FGF9 genes in the liver. In conclusion, dietary supplementation with MSM and Se-Y can effectively reduce the FLS of laying hens in the late peak laying period and increase their antioxidant capacity. The underlying biological mechanism may be related to the downregulation of genes involved in liver oxidative phosphorylation and inflammation-related pathways.

This study aimed to evaluate the effects of the spontaneous genetic mutation T329S in flavin-containing monooxygenase 3 (FMO3) on atherosclerosis (AS), fatty liver syndrome (FLS), and adiposity in 90-week-old layers. At 90 weeks of age, 27 FMO3 genotyped Rhode Island White chickens (consisting of nine AA hens, nine AT hens, and nine TT hens) with normal laying performance were selected. The AS lesions, incidence of FLS, fat deposition, metabolic characteristics, and production performance of these egg-layers with different FMO3 genotypes were assessed. The T329S mutation in TT hens reduced the AS lesions (P < 0.01) and altered the plasma metabolic indices more than it did in the AA and AT hens. Furthermore, it reduced the incidence of FLS, hepatic triglyceride deposition (P < 0.05), liver indices (P < 0.05), and fat deposition (P < 0.05) in the subcutis and abdomen of TT hens compared to those of AA and AT hens. Moreover, as an effect of T329S, TT hens laid a higher than average number of eggs and maintained a higher egg-laying rate from 68 to 90 weeks than AA and AT hens. Our study confirmed that the T329S mutation in FMO3 could reduce the development of AS lesions, the incidence of FLS, and fat deposition, which are associated with changes in plasma and hepatic metabolic indices and improvements in the laying performance of older layers. Our results may provide a new strategy for using the T329S mutation to improve the health status and production performance of layers during the late laying period.

In the present study, we sampled sea bream and sea bass, weighing 400-450g, for routine microbiological, hematological, macroscopical and histopathological examinations. Samples were taken from seemingly healthy fish, which displayed increased feed conversion rates, signs of cold shock and slow movement. Routine bacteriological analyses included basic microbiological analyses for oxidase and catalase activity, Gram staining and O/F fermentation using API test kits. Furthermore, 16S rRNA gene sequencing was performed for identification. Serum biochemical and hematological values were determined using a Vetscan®VS2 analyzer and blood smears. Internal organs were examined by routine histopathological techniques. Hepatic fat accumulation and necrosis were noted, and liver damage was observed to be associated with significant alterations in liver enzymes. Due to multi-organ dysfunction and serious hematological disorders, primarily Vibrio alginolyticus also Alteromonas and Pseudoalteromonas species were isolated from the affected fish and co-infections were detected. [ABSTRACT FROM AUTHOR]

Background: Glucocorticoid receptor (GR) mediated corticosterone-induced fatty liver syndrome (FLS) in the chicken by transactivation of Fat mass and obesity associated gene (FTO), leading to demethylation of N6-methyladenosine (m6A) and post-transcriptional activation of lipogenic genes. Nutrition is considered the main cause of FLS in the modern poultry industry. Therefore, this study was aimed to investigate whether GR and m6A modification are involved in high-energy and low protein (HELP) diet-induced FLS in laying hens, and if true, what specific m6A sites of lipogenic genes are modified and how GR mediates m6A-dependent lipogenic gene activation in HELP diet-induced FLS in the chicken. Results: Laying hens fed HELP diet exhibit excess (P < 0.05) lipid accumulation and lipogenic genes activation in the liver, which is associated with significantly increased (P < 0.05) GR expression that coincided with global m6A demethylation. Concurrently, the m6A demethylase FTO is upregulated (P < 0.05), whereas the m6A reader YTHDF2 is downregulated (P < 0.05) in the liver of FLS chickens. Further analysis identifies site-specific demethylation (P < 0.05) of m6A in the mRNA of lipogenic genes, including FASN, SREBP1 and SCD. Moreover, GR binding to the promoter of FTO gene is highly enriched (P < 0.05), while GR binding to the promoter of YTHDF2 gene is diminished (P < 0.05). Conclusions: These results implicate a possible role of GR-mediated transcriptional regulation of m6A metabolic genes on m6A-depenent post-transcriptional activation of lipogenic genes and shed new light in the molecular mechanism of FLS etiology in the chicken. [ABSTRACT FROM AUTHOR]

In order to assess the welfare and health status of commercial free-range laying hens of different body weight quantiles, a total of 7708 Lohmann Brown-classic hens at 74 weeks of age were obtained from 4 commercial freerange flocks housed on the same Australian farm under the same housing conditions. All hens were humanely killed and evaluated for body weight, feather cover, keel bone damage, gastrointestinal parasites, liver appearance, and egg follicle status. Hens were classified according to their body weight distribution percentile as light (bottom quartile, 1.65 ± 0.002 kg), medium (middle quartiles, 1.86 ± 0.010 kg), and heavy (top quartile, 2.08 ± 0.002 kg). All parameters were analysed using nominal regression models with flock, body weight, and their interactions as the predictors. In summary, 55.8% of heavy hens had a single or multiple keel bone damage compared to 48.9% and 50.7% of medium and light hens, respectively (P = 0.0001). Light hens had a significantly (P = 0.001) higher feather cover score on their breast (3.02 ± 0.018) than medium (2.96 ± 0.013) and heavy hens (2.87 ± 0.018) but significantly lower neck feather scores (P = 0.007). Light hens had the highest prevalence of gastrointestinal helminth infection (P = 0.0001), compared to the medium and heavy hens. Heavy hens had the highest incidence of Fatty Liver Syndrome compared to medium and light hens. Heavy and medium hens were significantly (P = 0.0001), more often in full egg follicle production (95.3% and 94.8%, respectively) compared to the lighter hens (90.0%). There was a significant flock effect for all parameters investigated. In conclusion, heavy (2.06 ± 0.010 kg) and medium (1.85 ± 0.010 kg) hens appeared healthier, more resilient towards infectious diseases and persistent in their egg follicle production. However, heavier hens suffered significantly more often from Fatty Liver Syndrome. Hens in the lowest quartile with mean 1.65 kg were the least economic sub-population. [ABSTRACT FROM AUTHOR]

Fatty liver syndrome (FLS) in laying hens is a metabolic disease that can potentially reduce egg production while compromising the health status of the bird. This study assessed the combined use of B vitamins via the feed (FLS-MIX) or the drinking water (FLS-LIQ) to reduce FLS and the use of spectrophotometry to estimate liver fat content. Individually, caged Hy-line brown hens (n = 288) underwent a pre-experimental period (from week 66 to 67, both included) receiving a Standard diet or a Challenge diet (high energy–low protein) to nutritionally induce the FLS. Subsequently, hens followed a 2 diets (Standard; Challenge) × 3 dietary supplements (NONE; FLS-MIX; and FLS-LIQ) factorial arrangement of treatments from 68 to 73 wk old, both included. Compared to the Standard, the Challenge diet increased liver fat (188 vs. 270 g/kg DM) and reduced feed consumption, lay percentage, and egg mass production (P < 0.05). No differences in lay performance or eggshell quality were observed among dietary supplements; however, FLS-MIX significantly increased (P < 0.05) feed intake relative to NONE. On birds subjected to the Challenge diet, the use of FLS-MIX and FLS-LIQ led to lower (P < 0.05) liver fat relative to NONE. Regression analysis between the L, a+, and b+ values and liver fat content provided significant (P < 0.001) regression equations to estimate liver fat content (R2 = 0.62). Results of this study suggest that B vitamin supplements could be an effective means to reduce liver fat deposition when hens are susceptible of suffering FLS, and that spectrometry could be a reliable tool to estimate liver fat content. [ABSTRACT FROM AUTHOR]

Metabolic dysfunction-associated fatty liver disease (MAFLD) and its interaction with many metabolic pathways raises global public health concerns. This study aimed to determine the therapeutic effects of Pyrroloquinoline quinone (PQQ, provided by PQQ.Na2) on MAFLD in a chick model and primary chicken hepatocytes with a focus on lipid metabolism, anti-oxidative capacity, and mitochondrial biogenesis. The MAFLD chick model was established on laying hens by feeding them a high-energy low-protein (HELP) diet. Primary hepatocytes isolated from the liver of laying hens were induced for steatosis by free fatty acids (FFA) and for oxidative stress by hydrogen peroxide (H2O2). In the MAFLD chick model, the dietary supplementation of PQQ conspicuously ameliorated the negative effects of the HELP diet on liver biological functions, suppressed the progression of MAFLD mainly through enhanced lipid metabolism and protection of liver from oxidative injury. In the steatosis and oxidative stress cell models, PQQ functions in the improvement of the lipid metabolism and hepatocytes tolerance to fatty degradation and oxidative damage by enhancing mitochondrial biogenesis and then increasing the anti-oxidative activity and anti-apoptosis capacity. At both the cellular and individual levels, PQQ was demonstrated to exert protective effects of hepatocyte and liver from fat accumulation through the improvement of mitochondrial biogenesis and maintenance of redox homeostasis. The key findings of the present study provide an in-depth knowledge on the ameliorative effects of PQQ on the progression of fatty liver and its mechanism of action, thus providing a theoretical basis for the application of PQQ, as an effective nutrient, into the prevention of MAFLD.

Fatty liver syndrome is a common metabolic disease that causes decrease in egg production and sudden death of laying hens. Phyllanthus urinaria (PU), a traditional herbal medicine, is widely used as anti-inflammatory and hepatoprotective medicine in Asia. The aim of this study was to investigate the effect of PU water extract on lipid accumulation and oxidative stress in an in vitro fatty liver syndrome model. Primary hepatocytes were isolated from 18 days of Lohmann embryonic chicks. Hepatocytes were cultured in medium with oleic acid (OA, 500 μM) or palmitic acid (PA, 200 μM) to induce lipid accumulation and oxidative stress respectively. Both experiments were treated with different concentration of PU water extract (0, 2, 10, 50 μg/mL) for 24 h. Metformin hydrochloride (1 mM) was used as a positive control. Cell viability, total triglycerides, TBARS, Oil red O staining, and mRNA expression of lipid metabolism-related genes were determined. The results indicated that PU water extract significantly decreased total triglycerides level (P < 0.05) in OA induced lipid accumulation. Moreover, treatment of PU water extract could downregulate the mRNA abundance of sterol regulatory element-binding protein 1 (SREBP1c), up-regulate the mRNA expression of carnitine palmitoyltransferase 1A (CPT1A) and peroxisome proliferator-activated receptor alpha (PPARa) in lipid accumulated hepatocytes. In oxidative stress experiment, PU water extract at the doses above 10 μg/mL of attenuated increase of malondialdehyde (MDA) abundance induced by PA (P < 0.05). We speculated that PU water extract effectively ameliorate lipid accumulation in primary chicken hepatocytes through decreasing of lipogenesis and increasing of beta-oxidation. PU water extract reduced lipid peroxidase, showing antioxidant effects. These results provide preliminary evidence for supporting PU water extract as a potential therapeutic agent to prevent and treat fatty liver syndrome in chickens. [ABSTRACT FROM AUTHOR]

Fatty liver syndrome is an emerging health problem in the world, due to the high prevalence of obesity and alcohol use disorder. Given the nature of the disease’s advancement to cirrhosis and liver-related complications, it is important to assess the severity of the disease, which is typically done via a liver biopsy. Due to the limitations and risks of liver biopsy, the role of noninvasive tests is essential and evolving to stratify the stage of the liver disease, predict the outcomes, and/or monitor the treatment response. This review is focused on noninvasive tests, including the use of serum-based biomarkers, ultrasound-based shear wave elastography, transient elastography, and magnetic resonance elastography in both clinical and research settings.

This experiment was conducted with male chicks to investigate the influence of hormones and nutrients on the development of fatty liver syndrome (FLS) as well as the effects of dietary lipotropic factors on hepatic fat accumulation and lipogenic enzyme gene expression. A total of two-hundred sixteen 4-wk-old Hy-Line male chicks were divided into six groups and fed an experimental diet (T1, low-energy diet with low levels of lipotropic factors; T2, high-energy diet with low levels of lipotropic factors; T3 and T5, low-energy diet with high levels of lipotropic factors; T4 and T6, high-energy diet with high levels of lipotropic factors) for six weeks. The chicks in T5 and T6 groups were treated with intramuscular injections of estradiol benzoate for three days prior to biopsy and clinical analysis of FLS. Chicks treated with estrogen had significantly greater liver weights than untreated chicks. The abdominal fat contents were increased in chicks consuming high-energy diets as compared to those consuming low-energy diets. Treatment with estrogen significantly increased the concentrations of serum cholesterol, triacylglycerol and phospholipid (p

High-producing dairy cows enter a period of negative energy balance during the first weeks of lactation. Energy intake is usually sufficient to cover the increase in energy requirements for fetal growth during the period before calving, but meeting the demand for energy is often difficult during the early stages of lactation. A catabolic state predominates during the transition period, leading to the mobilisation of energy reserves (NEFA and amino acids) that are utilised mainly by the liver and muscle. Increased uptake of mobilised NEFA by the liver, combined with the limited capacity of hepatocytes to either oxidise fatty acids for energy or to incorporate esterified fatty acids into VLDL results in fatty liver syndrome and ketosis. This metabolic disturbance can affect the general health, and it causes economic losses. Different nutritional strategies have been used to restrict negative effects associated with the energy challenge in transition cows. The provision of choline in the form of rumen-protected choline (RPC) can potentially improve liver function by increasing VLDL exportation from the liver. RPC increases gene expression of microsomal TAG transfer protein and APOB100 that are required for VLDL synthesis and secretion. Studies with RPC have looked at gene expression, metabolic hormones, metabolite profiles, milk production and postpartum reproduction. A reduction in liver fat and enhanced milk production has been observed with RPC supplementation. However, the effects of RPC on health and reproduction are equivocal, which could reflect the lack of sufficient dose-response studies. [ABSTRACT FROM AUTHOR]

Fatty liver syndrome is a metabolic disorder that occurs in mink (Mustela vison). The aim of this study was to compare the effects of dietary fat sources (chicken oil, fish oil and soybean oil) on the recovery fatty liver syndrome in female mink in response to short term fasting for 5 days and subsequent re-feeding for 7-28 days. Food deprivation resulted in the rapid mobilization of body fat, causing an elevated hepatosomatic index and increased liver lipid content. Re-feeding resulted in a more pronounced recovery of liver health in the mink fed the fish oil diet than chicken oil or soybean oil diet. The fish oil diet was found to be useful to relieve the severity of hepatic lipidosis in mink. [ABSTRACT FROM AUTHOR]

The experiment was conducted to investigate the effects of dihydropyridine supplementation on the laying performance and lipid metabolism of broiler breeder hens. A total of 720 forty-five week old broiler breeder hens were randomly divided into four experimental groups, each group consisting of six replicates of 30 birds. For 10 weeks the birds were fed a maize-soybean meal diet containing 0, 100, 200, 300 mg dihydropyridine/kg, in the respective treatment groups. The daily egg weight and daily feed intake were not affected by dihydropyridine supplementation, but the laying rate and feed efficiency were significantly increased. The percentage of abdominal fat and percentage of liver fat were significantly decreased by dietary dihydropyridine. A level of 100 mg dihydropyridine/kg had no effect on the hormone-sensitive triglyceride lipase (HSL) activity in the liver or abdominal fat, though higher levels of dietary dihydropyridine (200 mg/kg or 300 mg/kg) increased HSL activity in the liver and abdominal fat. The concentration of cyclic adenosine monophosphate (cAMP) and superoxide dismutase activity were significantly increased by dihydropyridine, but the malondialdehyde content decreased. The apolipoprotein B concentration was increased at levels of 100 and 200 mg dihydropyridine/kg, but the 300 mg level had no effect on apolipoprotein B, compared with the control group. The triiodothyronine concentration was significantly increased by dietary dihydropyridine. It is concluded that supplementing dihydropyridine in the diet has a beneficial effect on the laying performance and regulates the fat metabolism of broiler breeder hens. The results suggest that the supplementation of 200 mg dihydropyridine/kg diet is the optimal dose for broiler breeder hens. [ABSTRACT FROM AUTHOR]

The present study was conducted to determine the metal accumulation, antioxidant enzymatic response, hepatic intermediary metabolism and histological changes in Synechogobius hasta exposed to 0.35 (control), 9.7 and 19.2mg/L Zn, respectively, on the 0, 4th, 8th and 12th day. Waterborne Zn exposure significantly reduced hepatosomatic index, hepatic lipid contents and fatty liver occurrence rate, increased Zn, Fe and Mn contents and reduced the contents of Cu and Ca in liver, and increased muscle Zn content. Waterborne Zn exposure also significantly influenced enzymatic activities involved in antioxidant responses (superoxide dismutase, catalase, glutathione-S-transferase, malondialdehyde) in liver and spleen, and changed hepatic intermediary enzymatic activities (succinate dehydrogenase, malic dehydrogenase, lactate dehydrogenase, lipoprotein lipase, hepatic lipase), impaired the histological structure of the gill and spleen, and reduced vacuolated hepatocytes. Thus, our study demonstrated for the first time that waterborne Zn exposure could reduce fatty liver syndrome in S. hasta. [Copyright &y& Elsevier]

The present study was conducted to determine antioxidant responses, hepatic intermediary metabolism, histology and ultrastructure in Synechogobius hasta after a 15-days of waterborne cadmium (Cd) exposure at the concentrations of 0 (control), 0.10, 0.17 and 0.29mg Cd/l (corresponding to 0, 12.6%, 21.5% and 36.7% of 96h LC50), respectively. Growth performance and survival declined, but hepatosomatic index (HSI) increased with increasing waterborne Cd levels (P<0.05). Waterborne Cd exposure also significantly increased lipid contents in whole body and liver (P<0.05), and Cd accumulation in whole body, muscle and vertebrae. Waterborne Cd exposure changed hepatic enzymatic activities involved in intermediary metabolism, induced antioxidant responses and increased lipid peroxidation level in the gill, liver and spleen. Waterborne Cd exposure also caused considerable histological alterations of gill, liver and spleen, led ultrastructures damage of liver and spleen of fish, and induced fatty liver for this fish species. [Copyright &y& Elsevier]

The present study was conducted to determine growth, hepatic enzymatic activities and histology in Synechogobius hasta exposed to waterborne copper concentrations of 0 (control), 0.15 and 0.3mgCu/l, respectively, for 15 days, and explore whether waterborne copper exposure could induce the fatty liver syndrome for the fish species. Growth (WG and SGR) declined, but HSI increased in S. hasta with increasing waterborne copper levels (P<0.05). Waterborne copper exposure also significantly increased lipid content and reduced protein content in both whole body and liver, and increased copper accumulation in whole body and vertebrae. Copper exposure changed hepatic enzymatic activities (SOD, CAT, SDH, PK, LDH, LPL and HL) and increased hepatic lipid peroxidation level, impaired the histological structure of the gill and liver in S. hasta. Thus, our study demonstrated for the first time that waterborne Cu exposure could induce fatty liver syndrome in fish. [Copyright &y& Elsevier]

Given the very difficult odyssey of my early years, who could have imagined the incredible arid successful journey that constituted my life path after age 13? I was born into a Jewish family in Breslau, Germany, right before the rise of Nazism and Hider's election. After Kristallnacht, when my father was taken to Buchenwald Concentration Camp, we had to leave Germany as soon as possible. The first opportunity came in May of 1939, when we boarded the SS St. Louis bound for Havana. Cuba. Almost all passengers were denied entrance into Cuba, and the ship had to go back to Europe, where I ended up in France. In December of 1939, during World War II, I was fortunate to be able to leave France. This time I made it to Cuba, where my father was already in residence. A year later, my entire family was allowed into the United States. I took advantage of all the educational resources in this land of opportunity. I graduated valedictorian of my high school class and earned a four-year scholarship to Rutgers University, where I obtained a Bachelor of Science degree. I went on to earn a Master's Degree from the University of Connecticut and finally a PhD from the University of Illinois. Within two months after graduating from Illinois, I was hired as an assistant professor of nutritional biochemistry at Rutgers, where I enjoyed a most productive research and teaching career. My PhD research involved tryptophan and niacin metabolism in the chick, and upon arrival at Rutgers I continued amino acid studies with the goal of assessing the essential amino acid requirements for egg production. This research was crowned with success and was followed with amino acid requirement studies for maintenance and for growth in rabbits, and ultimately with a reevaluation of requirements in adult humans. An outgrowth of the maintenance requirements led to a series of investigations into the metabolism of histidine, histamine, and carnosine (a histidine-containing dipeptide). Histanune, we found, plays an important role in wound healing and stress management. Pyridoxal phosphate is the cofactor for the enzyme histidine decarhoxylase required for histamine synthesis and similarly serves as a cofactor for hydroxytryptophan decarboxylase, the enzyme that is pan of the pathway to serotonin synthesis. Investigations into these pathways led to interesting findings: brain concentrations of serotonin could be increased by supplementing the diet of rats with tryptophan and pyridoxine; the elevated brain serotonin levels had behavioral consequences. Alcohol craving, addiction, and withdrawal symptoms are affected by serotonin concentrations in the brain, and alleviation of these conditions can be achieved with simultaneous administration of serotonin and dopamine agonists. In the midst of our early amino acid studies, we serendipitously also became involved with lipid metabolism in relation to atherosclerosis and blood cholesterol in a chicken model. This work led to the recognition that soluble fibers, like pectin, had strong cholesterol-lowering properties that were beneficial in lowering the incidence of coronary plaque formation. The research success that I have enjoyed has well coupled with the gift of three accomplished children who are making important contributions as professionals in their fields of endeavor. My wife and I are also blessed with 10 wonderful grandchildren, our pride and joy! [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the effects of the spontaneous genetic mutation T329S in flavin-containing monooxygenase 3 (FMO3) on atherosclerosis (AS), fatty liver syndrome (FLS), and adiposity in 90-week-old layers. At 90 weeks of age, 27 FMO3 genotyped Rhode Island White chickens (consisting of nine AA hens, nine AT hens, and nine TT hens) with normal laying performance were selected. The AS lesions, incidence of FLS, fat deposition, metabolic characteristics, and production performance of these egg-layers with different FMO3 genotypes were assessed. The T329S mutation in TT hens reduced the AS lesions ( P < 0.01) and altered the plasma metabolic indices more than it did in the AA and AT hens. Furthermore, it reduced the incidence of FLS, hepatic triglyceride deposition ( P < 0.05), liver indices ( P < 0.05), and fat deposition ( P < 0.05) in the subcutis and abdomen of TT hens compared to those of AA and AT hens. Moreover, as an effect of T329S, TT hens laid a higher than average number of eggs and maintained a higher egg-laying rate from 68 to 90 weeks than AA and AT hens. Our study confirmed that the T329S mutation in FMO3 could reduce the development of AS lesions, the incidence of FLS, and fat deposition, which are associated with changes in plasma and hepatic metabolic indices and improvements in the laying performance of older layers. Our results may provide a new strategy for using the T329S mutation to improve the health status and production performance of layers during the late laying period., Competing Interests: GL and YY was employed by Beijing Huadu Yukou Poultry Industry Co. Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Song, Shi, Li, Liang, Zeng, Li, Yan, Xu and Zheng.)

The present study was designed to evaluate the effects of high dietary fat on serum cholesterol and fatty liver syndrome in broilers. For this purpose, 90 day-old chicks were divided into three equal groups A, B and C. Group A acted as control. The birds of group B were fed on diet containing vegetable fat while birds of group C were fed on diet containing animal fat. It was observed that the serum cholestrol values in chicks of groups B and C were higher than those of the control group. Furthermore, the serum cholesterol value was higher in birds of group C than group B. Grossly, the livers of birds of groups B and C were enlarged, pale in colour, soft in consistency and were having petechial haemorrhages with fat and fibrin deposits. Histopathologically, livers of groups B and C showed fatty infiltration, haemorrhages and mass of eosinophilic materials. The vacuoles coalesced to create clear space that displaced the nucleus to the periphery of the cell. It was concluded that addition of dietary fat from animal and vegetable sources in the diet of broiler chicks not only resulted in increase in serum cholesterol but also in marked macroscopic and microscopic changes in liver.

Metabolic dysfunction-associated fatty liver disease (MAFLD) and its interaction with many metabolic pathways raises global public health concerns. This study aimed to determine the therapeutic effects of Pyrroloquinoline quinone (PQQ, provided by PQQ.Na2) on MAFLD in a chick model and primary chicken hepatocytes with a focus on lipid metabolism, anti-oxidative capacity, and mitochondrial biogenesis. The MAFLD chick model was established on laying hens by feeding them a high-energy low-protein (HELP) diet. Primary hepatocytes isolated from the liver of laying hens were induced for steatosis by free fatty acids (FFA) and for oxidative stress by hydrogen peroxide (H2O2). In the MAFLD chick model, the dietary supplementation of PQQ conspicuously ameliorated the negative effects of the HELP diet on liver biological functions, suppressed the progression of MAFLD mainly through enhanced lipid metabolism and protection of liver from oxidative injury. In the steatosis and oxidative stress cell models, PQQ functions in the improvement of the lipid metabolism and hepatocytes tolerance to fatty degradation and oxidative damage by enhancing mitochondrial biogenesis and then increasing the anti-oxidative activity and anti-apoptosis capacity. At both the cellular and individual levels, PQQ was demonstrated to exert protective effects of hepatocyte and liver from fat accumulation through the improvement of mitochondrial biogenesis and maintenance of redox homeostasis. The key findings of the present study provide an in-depth knowledge on the ameliorative effects of PQQ on the progression of fatty liver and its mechanism of action, thus providing a theoretical basis for the application of PQQ, as an effective nutrient, into the prevention of MAFLD. [ABSTRACT FROM AUTHOR]

Fatty liver syndrome is an emerging health problem in the world, due to the high prevalence of obesity and alcohol use disorder. Given the nature of the disease's advancement to cirrhosis and liver-related complications, it is important to assess the severity of the disease, which is typically done via a liver biopsy. Due to the limitations and risks of liver biopsy, the role of noninvasive tests is essential and evolving to stratify the stage of the liver disease, predict the outcomes, and/or monitor the treatment response. This review is focused on noninvasive tests, including the use of serum-based biomarkers, ultrasound-based shear wave elastography, transient elastography, and magnetic resonance elastography in both clinical and research settings. [ABSTRACT FROM AUTHOR]

This experiment was conducted with male chicks to investigate the influence of hormones and nutrients on the development of fatty liver syndrome (FLS) as well as the effects of dietary lipotropic factors on hepatic fat accumulation and lipogenic enzyme gene expression. A total of two-hundred sixteen 4-wk-old Hy-Line male chicks were divided into six groups and fed an experimental diet (T1, low-energy diet with low levels of lipotropic factors; T2, high-energy diet with low levels of lipotropic factors; T3 and T5, low-energy diet with high levels of lipotropic factors; T4 and T6, high-energy diet with high levels of lipotropic factors) for six weeks. The chicks in T5 and T6 groups were treated with intramuscular injections of estradiol benzoate for three days prior to biopsy and clinical analysis of FLS. Chicks treated with estrogen had significantly greater liver weights than untreated chicks. The abdominal fat contents were increased in chicks consuming high-energy diets as compared to those consuming low-energy diets. Treatment with estrogen significantly increased the concentrations of serum cholesterol, triacylglycerol and phospholipid (p<0.05). The hepatic triacylglycerol levels were tenfold higher in the estrogen treated chicks than in the untreated chicks. There were no significant differences in malondialdehyde levels between the treatment groups. Estrogen treatment dramatically increased the levels of fatty acid synthetase, acetyl-CoA carboxylase and ApoB mRNA. The results indicated that treatment with exogenous estrogen in growing male chicks induced hepatic fat accumulation, which might be partially due to increased lipogenic enzyme gene expression.