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Gestational diabetes mellitus is a condition marked by raised blood sugar levels and insulin resistance that usually occurs during the second or third trimester of pregnancy. According to the World Health Organization, hyperglycemia affects 16.9% of pregnancies worldwide. Dietary changes are the primarily alternative treatment for gestational diabetes mellitus. This paper aims to perform an exhaustive overview of the interaction between diet, gene expression, and the metabolic pathways related to insulin resistance. The intake of foods rich in carbohydrates can influence the gene expression of glycolysis, as well as foods rich in fat, can disrupt the beta-oxidation and ketogenesis pathways. Furthermore, vitamins and minerals are related to inflammatory processes regulated by the TLR4/NF-κB and one carbon metabolic pathways. We indicate that diet regulated gene expression of PPARα, NOS, CREB3L3, IRS, and CPT I, altering cellular physiological mechanisms and thus increasing or decreasing the risk of gestational diabetes. The alteration of gene expression can cause inflammation, inhibition of fatty acid transport, or on the contrary help in the modulation of ketogenesis, improve insulin sensitivity, attenuate the effects of glucotoxicity, and others. Therefore, it is critical to comprehend the metabolic changes of pregnant women with gestational diabetes mellitus, to determine nutrients that help in the prevention and treatment of insulin resistance and its long-term consequences.

Background: The conjugated linoleic acid (CLA) isomer cis-9, trans-11 is an anticarcinogen that inhibits cell proliferation and/or induces apoptosis of tumor cells. The objective of this study was to evaluate the expression of genes responsible for cell cycle regulation and apoptosis in tumor explants of mammary anaplastic carcinoma (AC) and mammary tubulopapillary carcinoma (TC) cultured in vitro with the CLA isomers cis-9, trans-11 and trans-10, cis-12. Methods: In this study we used mammary explants from two adult female dogs that revealed two types of malignant tumors: (a) anaplastic mammary carcinoma (AC) and (b) mammary tubulopapillary carcinoma (TC). The explants (n = 6 per treatment) had an average weight of 80.0 ± 2.0 mg and were cultured for 24 h in 35 mm culture plates under the following treatments: (a) Control: Culture medium + fatty acid free bovine serum albumin (BSA); (b) Culture medium + cis-9, trans-11 CLA (75 µM) diluted with fatty acid free bovine serum albumin (BSA), and; (c) Culture medium + trans-10, cis-12 CLA (75 µM) diluted with fatty acid free bovine serum albumin (BSA). After that, total RNA was extracted, complementary DNA was synthesized (cDNA), and quantitative analysis by real-time polymerase chain reaction (RT-qPCR) was conducted. Data were analyzed using the MIXED procedure of SAS. Results: Compared with the Control, the CLA trans-10, cis-12 treatment decreased expression of the gene encoding the p53 by 20% (P = 0.02), Caspase-3 by 25% (P = 0.06) and Bax by 51% (P = 0.001) in AC. The CLA cis-9, trans-11 increased the gene expression of proapoptotic protein Bax in TC by 68% (P = 0.01), but increased the expression of the antiapoptotic Bcl2 gene in AC by 72% (P = 0.006). Conclusion: The CLA cis-9, trans-11 stimulates apoptotic genes in mammary tubulopapillary carcinoma, but has a contrary effect on the anaplastic carcinoma, and the CLA trans-10, cis-12 stimulates cell cycle progression genes and may have an antiapoptotic effect, mainly in mammary anaplastic carcinoma. [ABSTRACT FROM AUTHOR]

A significant portion of global greenhouse gas emissions is attributed to methane (CH4), the primary greenhouse gas released by dairy animals. Thus, livestock farming has a new challenge in reducing enteric CH4 for sustainability. In anaerobic microbial ecosystems such as the rumen, carbohydrates are converted into short-chain, volatile fatty acids that animals use for energy and protein synthesis. It is, therefore, essential to understand rumen physiology, population dynamics, and diversity to target methanogens. Thus far, numerous CH4 mitigation strategies have been studied, including feeding management, nutrition, rumen modification, genetics, and other approaches for increasing animal production. As new molecular techniques are developed, scientists have more opportunities to select animals with higher genetic merit through next-generation sequencing. The amount of CH4 produced per unit of milk or meat can be permanently and cumulatively reduced through genetic selection. Developing eco-friendly and practical nutrigenomic approaches to mitigating CH4 and increasing ruminant productivity is possible using next-generation sequencing techniques. Therefore, this review summarizes current genetic and nutrigenomic approaches to reducing enteric CH4 production without posing any danger to animals or the environment.

Simple Summary: Stressor challenges can lead to oxidative stress that can negatively impact poultry health and production. Phytogenics may exert beneficial effects on performance and product quality and enhance the endogenous antioxidant system. Therefore, the aim of this study was to evaluate the effects of dietary inclusion levels of a phytogenic premix on the production performance and critical detoxification and antioxidant molecular responses in the duodenum of laying hens. The overall laying rate and egg mass were significantly increased by phytogenic premix inclusion compared with the non-supplemented control. Phytogenic inclusion beneficially affected the expression of critical genes related to detoxification and antioxidant capacity. In conclusion, using an analytical nutrigenomics approach, this study provides new knowledge that further supports the noted phytogenic benefits for layer production performance. This knowledge could provide a new basis for diet formulation strategies using phytogenics in commercial conditions with multiple stressor challenges. The aim of this study was to evaluate the effects of a phytogenic premix (PP) on the production performance and critical genes relevant to the detoxification (i.e., aryl hydrocarbon receptor pathway) and antioxidant (i.e., nuclear factor erythroid 2-related factor 2 pathway) response in the duodenum of laying hens. The PP was based on bioactive substances derived from ginger, lemon balm, oregano, and thyme (Anco FIT-Poultry). A total of 385 20 week old Hy-Line Brown layers were assigned to five dietary treatments with seven replicates of 11 hens each for a 12-week feeding trial. The experimental treatments included a corn–soybean meal basal diet with no PP (CON) or supplemented with PP at 500 (P500), 750 (P750), 1000 (P1000), and 1500 mg/kg diet (P1500). The overall (1–12 weeks) laying rate (p < 0.001) and egg mass (p = 0.008) were significantly increased in the P1000 group compared with the CON. At the duodenum, increasing dietary PP inclusion levels beneficially affected (p ≤ 0.05) the expression of the majority of the AhR and Nrf2 pathway genes studied. In conclusion, according to the gene expression analysis, PP inclusion resulted in a reduced requirement for detoxification and an increased antioxidant capacity, with most of the effects seen at the PP inclusion range of 750 to 1000 mg/kg diet. [ABSTRACT FROM AUTHOR]

BackgroundThe PNPLA3 p.I148M impact on fat accumulation can be modulated by nutrients. Niacin (Vitamin B3) reduced triglycerides synthesis in in vitro and in vivo NAFLD models.ObjectivesIn this study, we aimed to investigate the niacin-I148M polymorphism crosstalk in NAFLD patients and examine niacin’s beneficial effect in reducing fat by exploiting hepatoma cells with different PNPLA3 genotype.DesignWe enrolled 172 (Discovery cohort) and 358 (Validation cohort) patients with non-invasive and histological diagnosis of NAFLD, respectively. Dietary niacin was collected from food diary, while its serum levels were quantified by ELISA. Hepatic expression of genes related to NAD metabolism was evaluated by RNAseq in bariatric NAFLD patients (n = 183; Transcriptomic cohort). Hep3B (148I/I) and HepG2 (148M/M) cells were silenced (siHep3B) or overexpressed (HepG2I148+) for PNPLA3, respectively.ResultsIn the Discovery cohort, dietary niacin was significantly reduced in patients with steatosis ≥ 2 and in I148M carriers. Serum niacin was lower in subjects carrying the G at risk allele and negatively correlated with obesity. The latter result was confirmed in the Validation cohort. At multivariate analysis, the I148M polymorphism was independently associated with serum niacin, supporting that it may be directly involved in the modulation of its availability. siHep3B cells showed an impaired NAD biosynthesis comparable to HepG2 cells which led to lower niacin efficacy in clearing fat, supporting a required functional protein to guarantee its effectiveness. Conversely, the restoration of PNPLA3 Wt protein in HepG2I148+ cells recovered the NAD pathway and improved niacin efficacy. Finally, niacin inhibited de novo lipogenesis through the ERK1/2/AMPK/SIRT1 pathway, with the consequent SREBP1-driven PNPLA3 reduction only in Hep3B and HepG2I148M+ cells.ConclusionsWe demonstrated a niacin-PNPLA3 I148M interaction in NAFLD patients which possibly pave the way to vitamin B3 supplementation in those with a predisposing genetic background.

A significant portion of global greenhouse gas emissions is attributed to methane (CH4), the primary greenhouse gas released by dairy animals. Thus, livestock farming has a new challenge in reducing enteric CH4 for sustainability. In anaerobic microbial ecosystems such as the rumen, carbohydrates are converted into short-chain, volatile fatty acids that animals use for energy and protein synthesis. It is, therefore, essential to understand rumen physiology, population dynamics, and diversity to target methanogens. Thus far, numerous CH4 mitigation strategies have been studied, including feeding management, nutrition, rumen modification, genetics, and other approaches for increasing animal production. As new molecular techniques are developed, scientists have more opportunities to select animals with higher genetic merit through next-generation sequencing. The amount of CH4 produced per unit of milk or meat can be permanently and cumulatively reduced through genetic selection. Developing eco-friendly and practical nutrigenomic approaches to mitigating CH4 and increasing ruminant productivity is possible using next-generation sequencing techniques. Therefore, this review summarizes current genetic and nutrigenomic approaches to reducing enteric CH4 production without posing any danger to animals or the environment. [ABSTRACT FROM AUTHOR]

• Good gut function and health is a prerequisite for sustainable poultry production. • Phytogenics are valuable tools for the beneficial modulation of poultry gut health. • Phytogenics counteract the detrimental effects induced by stressor challenges. • Nutrigenomics based mechanistic evidence for phytogenic function. • Phytogenics align with the global sustainability initiatives. Phytogenics are bioactive plant components that are intensively researched for their beneficial effects on poultry performance and health. Ongoing nutrigenomic studies provide mechanistic evidence for phytogenic benefits at the cellular molecular level. Critical biomarkers for gut function and health have been shown to be responsive to stressor challenges as well as to phytogenic administration. In particular, it has been shown that phytogenics induce opposite effects to the detrimental ones induced by stressor challenges, thereby providing opportunities to alleviate the negative effects of stressors on poultry production and health. Therefore, credible promotion of poultry gut function and health via phytogenic administration results in better feed utilization, higher production, healthier products, better poultry welfare, less environmental impact and production sustainability respecting the circular economy and green deal initiatives. Furthermore, phytogenics as valuable parts of overall disease prevention strategies align with the One Health initiative for healthy humans, healthy animals and a healthy planet. [ABSTRACT FROM AUTHOR]

Obesity is a chronic disease characterized by abnormal or excessive fat accumulation that could impact an individual’s health; moreover, the World Health Organization (WHO) has declared obesity a global epidemic since 1997. In Latin America, in 2016, reports indicated that 24.2% of the adult population was obese. The environmental factor or specific behaviors like dietary intake or physical activity have a vital role in the development of a condition like obesity, but the interaction of genes could contribute to that predisposition. Hence, it is vital to understand the relationship between genes and disease. Indeed, genetics in nutrition studies the genetic variations and their effect on dietary response; while genomics in nutrition studies the role of nutrients in gene expression. The present review represents a compendium of the dietary behaviors in the Latin American environment and the interactions of genes with their single nucleotide polymorphisms (SNPs) associated with obesity, including the risk allele frequencies in the Latin American population. Additionally, a bibliographical selection of several studies has been included; these studies examined the impact that dietary patterns in Latin American environments have on the expression of numerous genes involved in obesity-associated metabolic pathways.

Caffeine, Toxicant Responsive Genes and PD In Vivo Study In 2008, Singh and team investigated the roles of nicotine and caffeine on toxicant responsive gene expression in MPTP-induced PD [[48]]. Neuroprotective Mechanisms of Caffeine x Gene Interaction for the Amelioration of PD The promising molecular integration linking caffeine, gene expressions and PD is currently under investigation. Keywords: caffeine; coffee; complementary medicine; gene expressions; nutrigenomic; Parkinson's disease EN caffeine coffee complementary medicine gene expressions nutrigenomic Parkinson's disease N.PAG N.PAG 15 08/29/22 20220801 NES 220801 1. Heavy caffeine intake with CC genotype reduced PD risk by 47%, while having GRIN2A rs4998386 T allele with light caffeine intake showed a trend of protectiveness, and the combination of heavy caffeine intake and GRIN2A rs4998386 TC genotype was associated with an overall 64% PD risk reduction. [Extracted from the article]

The aim of this study was to evaluate the effects of a phytogenic premix (PP) on the production performance and critical genes relevant to the detoxification (i.e., aryl hydrocarbon receptor pathway) and antioxidant (i.e., nuclear factor erythroid 2-related factor 2 pathway) response in the duodenum of laying hens. The PP was based on bioactive substances derived from ginger, lemon balm, oregano, and thyme (Anco FIT-Poultry). A total of 385 20 week old Hy-Line Brown layers were assigned to five dietary treatments with seven replicates of 11 hens each for a 12-week feeding trial. The experimental treatments included a corn–soybean meal basal diet with no PP (CON) or supplemented with PP at 500 (P500), 750 (P750), 1000 (P1000), and 1500 mg/kg diet (P1500). The overall (1–12 weeks) laying rate (p < 0.001) and egg mass (p = 0.008) were significantly increased in the P1000 group compared with the CON. At the duodenum, increasing dietary PP inclusion levels beneficially affected (p ≤ 0.05) the expression of the majority of the AhR and Nrf2 pathway genes studied. In conclusion, according to the gene expression analysis, PP inclusion resulted in a reduced requirement for detoxification and an increased antioxidant capacity, with most of the effects seen at the PP inclusion range of 750 to 1000 mg/kg diet.

The purpose of this study was to investigate the effects of high levels of Tenebrio molitor dietary inclusion (15%) on molecular mechanisms that influence poultry health in a broiler chicken diet. The global gene expression of four tissues (breast, liver, jejunum, and caecum) was evaluated using the RNA-Seq approach. The analysis of differentially expressed genes suggested that the use of Tenebrio molitor leads to the overexpression of genes related to protein elongation required for tissue growth and development in the gut and liver. It would also appear to contain nutrients that reduce the expression of genes related to the immune system and inflammation of the mucosa. The dietary inclusion of Tenebrio molitor in poultry could also lead to a possible inactivation of the growth factor and a reduction of tissue free-radicals. No genes alterations have been detected in liver RNA expression that would discourage the use of larvae in feeding broilers. [ABSTRACT FROM AUTHOR]

Toll-like receptors (TLRs) are pathogen recognition receptors, and primitive sources of innate immune response that also play key roles in the defense mechanism against infectious diseases. About 10 different TLRs have been discovered in chicken that recognize ligands and participate in TLR signaling pathways. Research findings related to TLRs revealed new approaches to understand the fundamental mechanisms of the immune system, patterns of resistance against diseases, and the role of TLR-specific pathways in nutrient metabolism in chicken. In particular, the uses of specific feed ingredients encourage molecular biologists to exploit the relationship between nutrients (including different phytochemicals) and TLRs to modulate immunity in chicken. Phytonutrients and prebiotics are noteworthy dietary components to promote immunity and the production of disease-resistant chicken. Supplementations of yeast-derived products have also been extensively studied to enhance innate immunity during the last decade. Such interventions pave the way to explore nutrigenomic approaches for healthy and profitable chicken production. Additionally, single-nucleotide polymorphisms in TLRs have shown potential association with few disease outbreaks in chickens. This review aimed to provide insights into the key roles of TLRs in the immune response and discuss the potential applications of these TLRs for genomic and nutritional interventions to improve health, and resistance against different fatal diseases in chicken. [ABSTRACT FROM AUTHOR]

Purpose: The human obesity susceptibility gene, FTO, associates with body mass and obesity in humans through regulation of energy expenditure and intake. We aimed to determine how fatty acids in plasma and in diet associate with FTO gene expression in subcutaneous and visceral adipose tissues. Methods: In this study, 97 participants aged ≥ 18 years were selected from patients admitted to the hospital for abdominal surgeries. Habitual dietary intake of participants was collected using a valid and reliable food frequency questionnaire (FFQ), from which the intake of fatty acids was quantified. Plasma fatty acids were assessed by gas–liquid chromatography. The mRNA expression of the FTO gene in visceral and subcutaneous adipose tissues obtained by biopsy was measured by Real-Time Quantitative Reverse Transcription PCR. Standardized β-coefficients were calculated by multivariable linear regression. Results: After adjusting for age, homeostasis model insulin resistance index (HOMA-IR), and body mass index, total fatty acid intake was significantly associated with FTO gene expression in visceral (STZβ = 0.208, P = 0.037) and subcutaneous (STZβ = 0.236, P = 0.020) adipose tissues. Dietary intake of monounsaturated fatty acid (MUFA) and polyunsaturated fatty acids (PUFA) had positive significant associations with the expression of FTO in visceral (STZβ = 0.227, P = 0.023; STZβ = 0.346, P < 0.001, respectively) and subcutaneous (STZβ = 0.227, P = 0.026; STZβ = 0.274, P = 0.006, respectively) adipose tissues. There were no associations between plasma fatty acids and FTO mRNA expression in either subcutaneous or visceral adipose tissues. Conclusion: The weak association of dietary total fatty acids, MUFA, and PUFA with FTO gene expression in both adipose tissues may highlight the importance of dietary fatty acids composition along with total fat intake in relation to FTO gene expression. [ABSTRACT FROM AUTHOR]

Caffeine is one of the predominant dietary components and psychostimulants present in coffee, a widely appreciated beverage. Corroborating epidemiological and laboratory evidence have suggested an inverse association between the dietary intakes of coffee and the risk of Parkinson’s Disease (PD). Growing attention has been paid to the impact of coffee consumption and genetic susceptibility to PD pathogenesis. Coffee is believed to play prominent roles in mediating the gene makeup and influencing the onset and progression of PD. The current review documents a current discovery of the coffee × gene interaction for the protective management of PD. The evidence underlying its potent impacts on the adenosine receptors (A2AR), estrogen receptors (ESR), heme oxygenase (HO), toxicant responsive genes, nitric oxide synthase (NOS), cytochrome oxidase (Cox), familial parkinsonism genetic susceptibility loci, bone marrow stromal cell antigen 1 (BST1), glutamate receptor gene and apolipoprotein E (APOE) genotype expressions is outlined. Furthermore, the neuroprotective mechanisms of coffee for the amelioration of PD are elucidated.

Introduction: Genetic load may indirectly influence on cardiovascular risk. This work aimed to analyze the influence of polymorphisms (APOA5 C56G-Ser19Trp, Prothrombin-G20210A, F5 Arg506Gln, MTHFR-C677T, LIPC-C-514T, LPA-I4300M, PPAR_ALPHA-L162V, APOA5-1131T > C, APOE-APOE2/3/4, and APOE-APOE2,3,4) in plasma triglyceride (TG) levels of patients ingesting plant sterols. Materials and Methods: Double-blind, crossover, controlled clinical trial was performed in 45 individuals (25 women). About 2.24 g sterols in milk and placebo milk were ingested daily during 3 weeks each, separated by a 2-week washout period. Blood draws and saliva genomic DNA was extracted. Results: APOA5-C56G-Ser19Trp, MTHFR-C677T, and PPAR_ALPHA-L162V greatly benefit from sterols intake. APOA5-C56G-Ser19Trp GG homozygous carriers lowered their TGs more than CG heterozygote carriers (P = 0.003). TT homozygous carriers of gene LIPC C-514T experienced an increase of TGs. Conclusions: Further studies are needed to establish which genotype combinations is the most protective against hypertriglyceridemia.

Stunting is a global health problem. Based on WHO data, there are 161 million children who experience stunting. Breastmilk supplementation in the form of Moringa oleifera leaves powder is known to be beneficial in suppressing the stunting incidence. Moringa oleifera leaves powder contains protein, micronutrients, and minerals such as calcium, iron, sodium, vitamins C and E, beta carotene, and antioxidants (flavonoid acids, phenolic acids, glucosinolates, isothiocyanates, and saponins). The use of Moringa oleifera leaves powder in stunting cases has been carried out, but further studies in the aspects of nutrigenomics and molecular biology have not been conducted. This study is a literature review of relevant articles from www.pubmed.com, www.sciencedirect.com, and scholar.google.com. The author used keywords "stunting", "nutrigenomics", "biomolecular", and "Moringa oleifera". Pathogenic microbe such as Shigella and pathogenic E. coli ingestion can cause changes in DNA sequences in the stunting pathogenesis. Moringa oleifera leave powder can pass through nutrigenomic and biomolecular mechanisms. Some macro and micromolecules of Moringa oleifera leaves powder such as folate plays a role in DNA methylation; vegetable protein and fatty acids act as promoters in DNA sequences; vitamins act as cofactors for enzymes, antioxidant, and antiinflammation. Seeing various potential mechanisms in the aspects of nutrigenomic and molecular biology, Moringa oleifera leaves powder can be used in overcoming stunting. Further research is needed to give more review about cytokines and molecules included in this literature review.

The frequent spread of infectious diseases, viral or bacterial that continually affects our world, poses the need to adopt increasingly powerful methods to overcome the ability of pathogens to adapt, evolve and reduce the effectiveness of traditional therapies. The recent pandemic from Covid19 has highlighted in all its drama because traditional methods of treatment cannot overcome the pathogenic load of this virus and even less will succeed in winning the next pandemics. This manuscript proposes a holistic approach in the fight against infections, which in addition to dealing with the pathologies in place with the traditional strategies of care and prevention, is aimed primarily at strengthening the immune system of people, using advanced technologies to achieve maximum effectiveness. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is one of the most common type of cancer and an important contributor to female mortality. Several genes and epigenetic modifications are involved in the development and progression of BC. Research in phytochemistry, nutrigenomics, and nutrigenetics has provided strong evidence that certain phytonutrients are able to modulate gene expression at transcriptional and post-transcriptional levels. Such phytonutrients may also be beneficial to prevent and treat BC. In this review, we will focus on the nutrigenomic effects of various phytochemicals including polyphenols, phytosterols, terpenoids, alkaloids, and other compounds from different sources. Overall, these phytonutrients are found to inhibit BC cell proliferation, differentiation, invasion, metastasis, angiogenesis, and induce apoptotic cell death by targeting various molecular pathways. They also alter epigenetic mechanisms and enhance the chemosensitivity and radiosensitivity of cancer cells. Such phytochemicals may be used for the effective management of BC patients in the clinical setting in the future. The present article aims to summarize the specific molecular pathways involved in the genetic effects of phytochemicals in BC.

Aiming to reduce feed costs, cottonseed oil (CSO) has been used as an alternative component in diets for broilers. However, this oil contains gossypol, an antinutritional agent that impacts the use of mineral elements, inhibits glucose uptake, and has a direct inhibitory action on intestinal enzymes. Nevertheless, toxic effects of gossypol can be prevented by the addition of iron salts, such as ferrous sulfate (FS), to the diet. This work was conducted to evaluate performance and gene expression of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the intestines of 21- and 42-day-old broilers fed 0, 2, 4, or 6% concentrations of CSO, with or without FS. All CSO diets led to weight gain (WG) at 21 D. At 42 D, an increase in WG and a decrease in feed conversion (FCR) in the diets containing FS were observed. In 21-day-old birds supplemented with 4% CSO and FS, an increase in GPx gene expression was observed when compared to the 6% level. Animals (42 day old) supplemented with 6% CSO and FS presented greater expression of SOD gene when compared to 2% CSO and FS. In addition, a higher GPx expression in broilers supplemented with 6% CSO and FS compared to 6% CSO without FS was achieved. In conclusion, including CSO in the diets of broiler favors WG in animals at 21 D of age, independent of the presence or absence of FS; and including 4% CSO and FS in the diet of these animals alters the expression of the GPx gene in the intestine, so it is not necessary to add FS at 21 D. On the other hand, in 42-day-old broilers, the addition of FS is indicated, due to increases WG, decreased FCR and at the 6% CSO level without FS increase in the expression of the SOD and GPx genes. [ABSTRACT FROM AUTHOR]

Background: The Mediterranean diet, which is rich in olive oil, nuts, and fish, is considered healthy and may reduce the risk of chronic diseases. Methods: Here, we compared the transcriptome from the blood of subjects with diets supplemented with olives, nuts, or long-chain omega-3 fatty acids and identified the genes differentially expressed. The dietary genes obtained were subjected to network analysis to determine the main pathways, as well as the transcription factors and microRNA interaction networks to elucidate their regulation. Finally, a gene-associated disease interaction network was performed. Results: We identified several genes whose expression is altered after the intake of components of the Mediterranean diets compared to controls. These genes were associated with infection and inflammation. Transcription factors and miRNAs were identified as potential regulators of the dietary genes. Interestingly, caspase 1 and sialophorin are differentially expressed in the opposite direction after the intake of supplements compared to Alzheimer’s disease patients. In addition, ten transcription factors were identified that regulated gene expression in supplemented diets, mild cognitive impairment, and Alzheimer’s disease. Conclusions: We identified genes whose expression is altered after the intake of the supplements as well as the transcription factors and miRNAs involved in their regulation. These genes are associated with schizophrenia, neoplasms, and rheumatic arthritis, suggesting that the Mediterranean diet may be beneficial in reducing these diseases. In addition, the results suggest that the Mediterranean diet may also be beneficial in reducing the risk of dementia.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries and expose patients to increased risk of hepatic and cardiovascular (CV) morbidity and mortality. Both environmental factors and genetic predisposition contribute to the risk. An inappropriate diet, rich in refined carbohydrates, especially fructose, and saturated fats, and poor in fibers, polyunsaturated fats, and vitamins is one of the main key factors, as well as the polymorphism of patatin-like phospholipase domain containing 3 (PNPLA3 gene) for NAFLD and the apolipoproteins and the peroxisome proliferator-activated receptor (PPAR) family for the cardiovascular damage. Beyond genetic influence, also epigenetics modifications are responsible for various clinical manifestations of both hepatic and CV disease. Interestingly, data are accumulating on the interplay between diet and genetic and epigenetic modifications, modulating pathogenetic pathways in NAFLD and CV disease. We report the main evidence from literature on the influence of both macro and micronutrients in NAFLD and CV damage and the role of genetics either alone or combined with diet in increasing the risk of developing both diseases. Understanding the interaction between metabolic alterations, genetics and diet are essential to treat the diseases and tailoring nutritional therapy to control NAFLD and CV risk.

The long-term sustainability of aquaculture depends on finding economically viable and environmentally friendly feed ingredients to reduce the use of fishmeal and fish oil. An optimal strategy for the industry is not to identify substitutes or alternatives, but to find a combination of complementary raw materials that together meet the specific nutritional requirements for a given farmed fish species. The study aimed to examine the effects of different diets on the pyloric caeca and distal intestine of subadult European seabass (Dicentrarchus labrax) by applying transcriptomics and transmission electron microscopy. The study examined three dietary approaches: the classic fishmeal-based diet, a plant-based diet, and a plant-insect-poultry-based diet. The distal intestine was more sensitive to dietary changes than the pyloric caeca. The differentially expressed genes in both experimental diets were mainly involved in the digestion and absorption of proteins, fats, and vitamins. The overall transcriptomic changes were greater in the plant-based group than in the plant-insect-poultry-based group and included a greater number of overrepresented metabolic and signalling pathways. In contrast to the transcriptomic results, the ultrastructural findings showed decreased inflammation and/or evidence of tissue repair in the plant-based group, particularly in the pyloric caeca. Since the nutritional quality of all fish groups in this study was previously evaluated positively, the detected transcriptome-level changes can serve as evidence supporting the efficient nutrient utilisation and adaptability in European seabass. The study provides valuable insight into the potential benefits and implications of these dietary modifications on intestinal health and pathway regulation in European seabass. This can serve as a basis for further development of sustainable European seabass aquaculture practices and optimisation of diet formulations. • Novel dietary approaches: Plant-based diets with complementary non-fish ingredients. • Overall transcriptomic changes greater in the plant-based diet group. • Gut specialisation: Distal intestine showed stronger response than pyloric caeca. • Ultrastructural analysis: Reduced inflammation noted in the plant-based diet group. • Sustainable implication: Insights for optimising European seabass aquaculture diets. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus is a condition marked by raised blood sugar levels and insulin resistance that usually occurs during the second or third trimester of pregnancy. According to the World Health Organization, hyperglycemia affects 16.9% of pregnancies worldwide. Dietary changes are the primarily alternative treatment for gestational diabetes mellitus. This paper aims to perform an exhaustive overview of the interaction between diet, gene expression, and the metabolic pathways related to insulin resistance. The intake of foods rich in carbohydrates can influence the gene expression of glycolysis, as well as foods rich in fat, can disrupt the beta-oxidation and ketogenesis pathways. Furthermore, vitamins and minerals are related to inflammatory processes regulated by the TLR4/NF-κB and one carbon metabolic pathways. We indicate that diet regulated gene expression of PPARα , NOS , CREB3L3 , IRS , and CPT I , altering cellular physiological mechanisms and thus increasing or decreasing the risk of gestational diabetes. The alteration of gene expression can cause inflammation, inhibition of fatty acid transport, or on the contrary help in the modulation of ketogenesis, improve insulin sensitivity, attenuate the effects of glucotoxicity, and others. Therefore, it is critical to comprehend the metabolic changes of pregnant women with gestational diabetes mellitus, to determine nutrients that help in the prevention and treatment of insulin resistance and its long-term consequences., Competing Interests: The 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 © 2023 Guevara-Ramírez, Paz-Cruz, Cadena-Ullauri, Ruiz-Pozo, Tamayo-Trujillo, Felix, Simancas-Racines and Zambrano.)

Penelitian genom yang mengkaji kaitan antara setiap gen dengan suatu penyakit sekaligus mekanismenya untuk mendapatkan pengetahuan yang menyeluruh dalam pengobatan, telah membawa perubahan besar dunia kedokteran dalam mengobati berbagai penyakit. Namun demikian, penelitian genom seharusnya tidak hanya dimanfaatkan untuk pengobatan tetapi juga untuk pencegahan penyakit. Artikel ini membahas masalah kesehatan masyarakat dan peluang pemanfaatan penelitian genom dalam pencegahan penyakit. Penelitian genom yang dapat dimanfaatkan pada bidang kesehatan masyarakat adalah toksikogenomik dan nutrigenomik. Penelitian toksikogenomik mengkaji respons gen akibat pajanan toksikan yang berdampak pada kesehatan manusia. Penelitian nutrigenomik mengkaji respons gen terhadap makanan yang berdampak pada kesehatan manusia. Penelitian toksikogenomik dan nutrigenomik dapat mengungkap mekanisme molekuler suatu penyakit. Selanjutnya, pada gen yang mengalami perubahan ekspresi dapat dijadikan target molekuler untuk pencegahan. Dengan demikian, perkembangan penelitian genom memberikan tantangan bagi pengembangan ilmu kesehatan masyarakat untuk dalam pencegahan penyakit. Genome research which examines association of each gene with a disease and its mechanism to explore comprehensive knowledge in disease treatment, has brought about great changes in medicine in the treatment of diseases. However, genomic research should not only be applied in treatment but also in disease prevention. This article discusses public health problems and opportunities of genomic research application in disease prevention. Genome research that can be utilized in the field of public health is toxicogenomics and nutrigenomics. Research toxicogenomics investigate gene responses due to exposure to the toxicant that impact on human health. Nutrigenomics research examines gene response to food that affect to human health. Toxicogenomics and nutrigenomics research can uncover the molecular mechanisms of disease. Furthermore, the gene expression changes that may be used as molecular targets for prevention. Thus, the development of genome research provides a challenge for the development of public health sciences to be used in the prevention of disease.

Human nutrition is a branch of medicine based on foods biochemical interactions with the human body. The phenotypic transition from health to disease status can be attributed to changes in genes and/or protein expression. For this reason, a new discipline has been developed called “-omic science”. In this review, we analyzed the role of “-omics sciences” (nutrigenetics, nutrigenomics, proteomics and metabolomics) in the health status and as possible therapeutic tool in chronic degenerative diseases. In particular, we focused on the role of nutrigenetics and the relationship between eating habits, changes in the DNA sequence and the onset of nutrition-related diseases. Moreover, we examined nutrigenomics and the effect of nutrients on gene expression. We perused the role of proteomics and metabolomics in personalized nutrition. In this scenario, we analyzed also how dysbiosis of gut microbiota can influence the onset and progression of chronic degenerative diseases. Moreover, nutrients influencing and regulating gene activity, both directly and indirectly, paves the way for personalized nutrition that plays a key role in the prevention and treatment of chronic degenerative diseases.

Consistent evidence from both experimental and human studies indicates that Type 2 diabetes mellitus (T2DM) is a complex disease resulting from the interaction of genetic, epigenetic, environmental, and lifestyle factors. Nutrients and dietary patterns are important environmental factors to consider in the prevention, development and treatment of this disease. Nutritional genomics focuses on the interaction between bioactive food components and the genome and includes studies of nutrigenetics, nutrigenomics and epigenetic modifications caused by nutrients. There is evidence supporting the existence of nutrient-gene and T2DM interactions coming from animal studies and family-based intervention studies. Moreover, many case-control, cohort, cross-sectional cohort studies and clinical trials have identified relationships between individual genetic load, diet and T2DM. Some of these studies were on a large scale. In addition, studies with animal models and human observational studies, in different countries over periods of time, support a causative relationship between adverse nutritional conditions during in utero development, persistent epigenetic changes and T2DM. This review provides comprehensive information on the current state of nutrient-gene interactions and their role in T2DM pathogenesis, the relationship between individual genetic load and diet, and the importance of epigenetic factors in influencing gene expression and defining the individual risk of T2DM. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. Micronutrients modulate the immune system and exert a protective action by reducing low-density lipoproteins oxidation (ox-LDL) via induction of antioxidant enzymes. SUBJECTS AND METHODS: The clinical study was a randomized and cross-over trial, conducted through the CONSORT flowchart. We evaluated the gene expression of 103 genes related to oxidative stress (HOSp) and human inflammasome pathways (HIp), and ox-LDL level at fasting and after 40 g raw "Tonda Gentile delle Langhe" hazelnut consumption, in association with a McDonald's® Meal (McDM) in 22 healthy human volunteers. RESULTS: Ox-LDL levels significantly increased comparing no dietary treatment (NDT) vs. McDM, and decreased comparing McDM vs. McDM + H (p<0.05). Percentage of significant genes expressed after each dietary treatment were the follows: (A) NDT vs. McDM: 3.88% HIp and 17.48% HOSp; (B) NDT vs. McDM + H: 17.48% HIp and 23.30% HOSp; (C) McDM vs. McDM + H: 17.48% HIp and 33.98% HOSp. CONCLUSIONS: Hazelnut consumption reduced post prandial risk factors of atheroscle-rosis, such as ox-LDL, and the expression of inflammation and oxidative stress related genes. Chronic studies on larger population are necessary before definitive conclusions. [ABSTRACT FROM AUTHOR]

Aims: Inflammation and oxidative damage contribute significantly to the development of cardiovascular diseases (CVD). Postprandial oxidative stress and inflammation are characterized by an increased susceptibility of the organism toward oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. Micronutrients modulate immune system and exert a protective action by reducing oxidized low-density lipoprotein (ox-LDL) level. The aim of the present study was to evaluate the postprandial plasma ox-LDL level and the gene expression of 13 genes related to oxidative stress (HOSp) and human inflammasome pathways (HIp), after a tocopherol-enriched Mediterranean meal (TEM), and a Western high-fat meal (HFM). Moreover, Mediterranean Adequacy Index was calculated to define the quality of both meals. Methods: We set up a randomized and crossover trial in healthy human volunteers. Ox-LDL level was measured by enzyme-linked immunosorbent assay and the gene expression of 13 genes related to HOSp and HIp by qRT-PCR. Results: Ox-LDL levels significantly decreased comparing HFM versus TEM ( p < 0.05). Percentages of significantly overexpressed genes after each dietary treatment are as follows: (A) baseline versus HFM: 7.69 % HIp and 23.08 % HOSp; (B) baseline versus TEM: 7.69 % HIp and 7.69 % HOSp; (C) HFM versus TEM: 15.38 % HIp and 15.38 % HOSp. Conclusions: TEM reduced postprandial risk factors of CVD, such as ox-LDL, and the expression of inflammation and oxidative stress-related genes. Chronic studies on larger population are necessary before definitive conclusions. Trial registration: ClinicalTrials.gov Id: NCT01890070. [ABSTRACT FROM AUTHOR]

Celiac disease (CD), a common heritable chronic inflammatory condition of the small intestine caused by permanent intolerance to gluten/gliadin (prolamin), is characterized by a complex interplay between genetic and environmental factors. Developments in proteomics have provided an important contribution to the understanding of the biochemical and immunological aspects of the disease and the mechanisms involved in toxicity of prolamins. It has been demonstrated that some gliadin peptides resistant to complete proteolytic digestion may directly affect intestinal cell structure and functions by modulating gene expression and oxidative stress. In recent years, the creation of the two research fields Nutrigenomics and Nutrigenetics, has enabled the elucidation of some interactions between diet, nutrients and genes. Various dietary components including long chain ω-3 fatty acids, plant flavonoids, and carotenoids have been demonstrated to modulate oxidative stress, gene expression and production of inflammatory mediators. Therefore their adoption could preserve intestinal barrier integrity, play a protective role against toxicity of gliadin peptides and have a role in nutritional therapy of celiac disease.

Background: The PNPLA3 p.I148M impact on fat accumulation can be modulated by nutrients. Niacin (Vitamin B3) reduced triglycerides synthesis in in vitro and in vivo NAFLD models., Objectives: In this study, we aimed to investigate the niacin-I148M polymorphism crosstalk in NAFLD patients and examine niacin's beneficial effect in reducing fat by exploiting hepatoma cells with different PNPLA3 genotype., Design: We enrolled 172 (Discovery cohort) and 358 (Validation cohort) patients with non-invasive and histological diagnosis of NAFLD, respectively. Dietary niacin was collected from food diary, while its serum levels were quantified by ELISA. Hepatic expression of genes related to NAD metabolism was evaluated by RNAseq in bariatric NAFLD patients ( n = 183; Transcriptomic cohort). Hep3B (148I/I) and HepG2 (148M/M) cells were silenced (siHep3B) or overexpressed (HepG2 I148 + ) for PNPLA3 , respectively., Results: In the Discovery cohort, dietary niacin was significantly reduced in patients with steatosis ≥ 2 and in I148M carriers. Serum niacin was lower in subjects carrying the G at risk allele and negatively correlated with obesity. The latter result was confirmed in the Validation cohort. At multivariate analysis, the I148M polymorphism was independently associated with serum niacin, supporting that it may be directly involved in the modulation of its availability. siHep3B cells showed an impaired NAD biosynthesis comparable to HepG2 cells which led to lower niacin efficacy in clearing fat, supporting a required functional protein to guarantee its effectiveness. Conversely, the restoration of PNPLA3 Wt protein in HepG2 I148 + cells recovered the NAD pathway and improved niacin efficacy. Finally, niacin inhibited de novo lipogenesis through the ERK1/2/AMPK/SIRT1 pathway, with the consequent SREBP1 -driven PNPLA3 reduction only in Hep3B and HepG2 I148M+ cells., Conclusions: We demonstrated a niacin-PNPLA3 I148M interaction in NAFLD patients which possibly pave the way to vitamin B3 supplementation in those with a predisposing genetic background., Competing Interests: The 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 © 2023 Paolini, Longo, Meroni, Tria, Cespiati, Lombardi, Badiali, Maggioni, Fracanzani and Dongiovanni.)

The aim of the present study was to generate an experimental model to characterize the nutrigenomic profile of a plant-derived nutritional stress. Atlantic salmon ( Salmo salar ) was used as the model species. The nutritional stress was induced by inclusion of dietary defatted soybean meal (SBM), as this ingredient had been previously demonstrated to induce enteropathy in the distal intestine and reduce growth in salmon. Triplicate groups of Atlantic salmon were fed concentrations of 0, 100, 200 and 300 g kg − 1 SBM for 12 weeks and reduced growth performance was used as the indicator of nutritional stress. The transcriptome was analyzed in two tissues, liver and distal intestine, with the hypothesis being that the liver transcriptome would be characterized by gene expression responses related to overall growth and health performance, whereas intestinal gene expression would be dominated by specific responses to SBM. A set of 133 genes was differentially expressed in liver including 44 genes in common with the intestinal response. The liver-specific response included up-regulation of genes involved in protein digestion, energy metabolism and immune functions, whereas genes in other metabolic pathways were generally anabolic and down-regulated. These responses may be more related to general nutritional stress than to SBM per se . The transcriptomic profile in the distal intestine was consistent with the enteritis response as described previously. This study provides a comprehensive report on the profiles of liver and distal intestine transcriptomes, specifically highlighting the role of the liver in fish undergoing SBM-induced nutritional stress. [ABSTRACT FROM AUTHOR]

Copper is an essential micronutrient for organism health. Dietary changes or pathologies linked to this metal induce changes in intracellular glutathione concentrations. Here, we studied the transcriptional activation of glutathione pathways in Jurkat cell lines, analyzing the effect of change in glucose homeostasis during a physiological and supra-physiological copper exposure. An immortalized line of human T lymphocyte cell line (Jurkat) was exposed to different copper and glucose conditions to mimic concentrations present in human blood. We applied treatments for 6 (acute) and 24 h (sustained) to 2 µM (physiological) or 20 µM (supra-physiological, Wilson disease scenario) of CuSO in combination with 25 mg/dL (hypoglycemia), 100 mg/dL (normal) and 200 mg/dL (hyperglycemia, diabetes scenario) of glucose. The results indicate that a physiological concentration of copper exposure does not induce transcriptional changes in the glutathione synthesis pathway after 6 or 24 h. The G6PDH gene (regeneration pathway), however, is induced during a supra-physiological copper condition. This data was correlated with the viability assays, where fluctuation in both glucose conditions (hypo and hyperglycemia scenario) affected Jurkat proliferation when 20 µM of CuSO was added to the culture media. Under a copper overload condition, the transcription of a component of glutathione regeneration pathway (G6PDH gene) is activated in cells chronically exposed to a hyperglycemia scenario, indicating that fluctuations in glucose concentration impact the resistance against the metal. Our findings illustrate the importance of glucose homeostasis during copper excess. [ABSTRACT FROM AUTHOR]

Obesity is a chronic disease characterized by abnormal or excessive fat accumulation that could impact an individual's health; moreover, the World Health Organization (WHO) has declared obesity a global epidemic since 1997. In Latin America, in 2016, reports indicated that 24.2% of the adult population was obese. The environmental factor or specific behaviors like dietary intake or physical activity have a vital role in the development of a condition like obesity, but the interaction of genes could contribute to that predisposition. Hence, it is vital to understand the relationship between genes and disease. Indeed, genetics in nutrition studies the genetic variations and their effect on dietary response; while genomics in nutrition studies the role of nutrients in gene expression. The present review represents a compendium of the dietary behaviors in the Latin American environment and the interactions of genes with their single nucleotide polymorphisms (SNPs) associated with obesity, including the risk allele frequencies in the Latin American population. Additionally, a bibliographical selection of several studies has been included; these studies examined the impact that dietary patterns in Latin American environments have on the expression of numerous genes involved in obesity-associated metabolic pathways., Competing Interests: The 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 Guevara-Ramírez, Cadena-Ullauri, Ruiz-Pozo, Tamayo-Trujillo, Paz-Cruz, Simancas-Racines and Zambrano.)

• This is the first systematic review on n-3 PUFA supplementation and the impact on telomeres. • n-3 PUFA supplementation had no statistically significant effect on telomere length. • n-3 PUFA supplementation showed a tendency to reduce telomere attrition. • Different activity of the telomerase enzyme was observed in the studies. Evidence suggests antioxidant and anti-inflammatory properties of omega-3 polyunsaturated fatty acids (n-3 PUFA). However, the effect of supplementation of this fatty acid profile on the telomere length and the telomerase enzyme activity was not revised yet. The PubMed and Embase® databases were used to search for clinical trials. A total of six clinical trials were revised. Omega-3 PUFA supplementation did not statistically affect telomere length in three out of three studies but affected telomerase activity in two out of four studies. The supplementation increased telomerase enzyme activity in subjects with first-episode schizophrenia. Besides, it decreased telomerase enzyme activity without modulating the effects of Pro12Ala polymorphism on the PPARγ gene in type 2 diabetes subjects. The methodological differences between the studies and the limited number of studies on the theme suggest that further studies are needed to elucidate the effects of n-3 PUFA supplementation on telomere length and telomerase enzyme activity in humans. [ABSTRACT FROM AUTHOR]