Nutrient-Gene Interactions
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PROVIDER: S-EPMC6265830 | biostudies-literature | 2018 Jun
REPOSITORIES: biostudies-literature
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Project description:A large number of genome-wide association studies, transferability studies, and candidate gene studies performed in diverse populations around the world have identified gene variants that are associated with common human obesity. The mounting evidence suggests that these obesity gene variants interact with multiple environmental factors and increase susceptibility to this complex metabolic disease. The objective of this review article is to provide concise and updated information on energy balance, heritability of body weight, origins of gene variants, and gene-nutrient interactions in relation to human obesity. It is proposed that knowledge of these related topics will provide valuable insight for future preventative lifestyle intervention using targeted nutritional and medicinal therapies.
| S-EPMC5663124 | biostudies-literature
Project description:Acetyl-CoA carboxylase β (ACC2) plays a key role in fatty acid synthesis and oxidation pathways. Disturbance of these pathways is associated with impaired insulin responsiveness and metabolic syndrome (MetS). Gene-nutrient interactions may affect MetS risk. This study determined the relationship between ACC2 polymorphisms (rs2075263, rs2268387, rs2284685, rs2284689, rs2300453, rs3742023, rs3742026, rs4766587, and rs6606697) and MetS risk, and whether dietary fatty acids modulate this in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). Minor A allele carriers of rs4766587 had increased MetS risk (OR 1.29 [CI 1.08, 1.58], P = 0.0064) compared with the GG homozygotes, which may in part be explained by their increased body mass index (BMI), abdominal obesity, and impaired insulin sensitivity (P < 0.05). MetS risk was modulated by dietary fat intake (P = 0.04 for gene-nutrient interaction), where risk conferred by the A allele was exacerbated among individuals with a high-fat intake (>35% energy) (OR 1.62 [CI 1.05, 2.50], P = 0.027), particularly a high intake (>5.5% energy) of n-6 polyunsaturated fat (PUFA) (OR 1.82 [CI 1.14, 2.94], P = 0.01; P = 0.05 for gene-nutrient interaction). Saturated and monounsaturated fat intake did not modulate MetS risk. Importantly, we replicated some of these findings in an independent cohort. In conclusion, the ACC2 rs4766587 polymorphism influences MetS risk, which was modulated by dietary fat, suggesting novel gene-nutrient interactions.
| S-EPMC2975722 | biostudies-literature
Project description:Type 2 diabetes mellitus (T2DM), like all chronic diseases, results from interactions between multiple genes and multiple environmental factors. Nevertheless, many research studies focus on either nutrition or genetic factors independently of each other. The challenges of analyzing gene-nutrient interactions in T2DM are the (i) genetic heterogeneity in humans, (ii) complexity of environmental factors, particularly dietary chemicals, and (iii) diverse physiologies that produce the same apparent disease. Many of these variables are not accounted for in the design or study of T2DM or, indeed, most chronic diseases, although exceptions are noteworthy. Establishing experimental paradigms to analyze the complexity of these interactions and physiologies is challenging, but possible. This article provides a strategy to extend nutrigenomic experimental strategies to include early environmental influences that may promote adult-onset disease.
| S-EPMC2769961 | biostudies-literature
Project description:BackgroundObesity is a complex metabolic disorder that is associated with several diseases. Recently, precision nutrition (PN) has emerged as a tailored approach to provide individualised dietary recommendations.AimThis review discusses the major intrinsic and extrinsic components considered when applying PN during the management of obesity and common associated chronic conditions.ResultsThe review identified three main PN components: gene-nutrient interactions, intestinal microbiota, and lifestyle factors. Genetic makeup significantly contributes to inter-individual variations in dietary behaviours, with advanced genome sequencing and population genetics aiding in detecting gene variants associated with obesity. Additionally, PN-based host-microbiota evaluation emerges as an advanced therapeutic tool, impacting disease control and prevention. The gut microbiome's composition regulates diverse responses to nutritional recommendations. Several studies highlight PN's effectiveness in improving diet quality and enhancing adherence to physical activity among obese patients. PN is a key strategy for addressing obesity-related risk factors, encompassing dietary patterns, body weight, fat, blood lipids, glucose levels, and insulin resistance.ConclusionPN stands out as a feasible tool for effectively managing obesity, considering its ability to integrate genetic and lifestyle factors. The application of PN-based approaches not only improves current obesity conditions but also holds promise for preventing obesity and its associated complications in the long term.
| S-EPMC10935146 | biostudies-literature
Project description:Advances in the development of bioinformatic tools continue to improve investigators' ability to interrogate, organize, and derive knowledge from large amounts of heterogeneous information. These tools often require advanced technical skills not possessed by life scientists. User-friendly, low-barrier-to-entry methods of visualizing nutrigenomics information are yet to be developed. We utilized concept mapping software from the Institute for Human and Machine Cognition to create a conceptual model of diet and health-related data that provides a foundation for future nutrigenomics ontologies describing published nutrient-gene/polymorphism-phenotype data. In this model, maps containing phenotype, nutrient, gene product, and genetic polymorphism interactions are visualized as triples of two concepts linked together by a linking phrase. These triples, or "knowledge propositions," contextualize aggregated data and information into easy-to-read knowledge maps. Maps of these triples enable visualization of genes spanning the One-Carbon Metabolism (OCM) pathway, their sequence variants, and multiple literature-mined associations including concepts relevant to nutrition, phenotypes, and health. The concept map development process documents the incongruity of information derived from pathway databases versus literature resources. This conceptual model highlights the importance of incorporating information about genes in upstream pathways that provide substrates, as well as downstream pathways that utilize products of the pathway under investigation, in this case OCM. Other genes and their polymorphisms, such as TCN2 and FUT2, although not directly involved in OCM, potentially alter OCM pathway functionality. These upstream gene products regulate substrates such as B12. Constellations of polymorphisms affecting the functionality of genes along OCM, together with substrate and cofactor availability, may impact resultant phenotypes. These conceptual maps provide a foundational framework for development of nutrient-gene/polymorphism-phenotype ontologies and systems visualization.
| S-EPMC4172641 | biostudies-literature
Project description:Long-chain acyl CoA synthetase 1 (ACSL1) plays an important role in fatty acid metabolism and triacylglycerol (TAG) synthesis. Disturbance of these pathways may result in dyslipidemia and insulin resistance, hallmarks of the metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genetic determinants of lipid metabolism to affect MetS risk. We investigated the relationship between ACSL1 polymorphisms (rs4862417, rs6552828, rs13120078, rs9997745, and rs12503643) and MetS risk and determined potential interactions with dietary fat in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1,754). GG homozygotes for rs9997745 had increased MetS risk {odds ratio (OR) 1.90 [confidence interval (CI) 1.15, 3.13]; P = 0.01}, displayed elevated fasting glucose (P = 0.001) and insulin concentrations (P = 0.002) and increased insulin resistance (P = 0.03) relative to the A allele carriers. MetS risk was modulated by dietary fat, whereby the risk conferred by GG homozygosity was abolished among individuals consuming either a low-fat (<35% energy) or a high-PUFA diet (>5.5% energy). In conclusion, ACSL1 rs9997745 influences MetS risk, most likely via disturbances in fatty acid metabolism, which was modulated by dietary fat consumption, particularly PUFA intake, suggesting novel gene-nutrient interactions.
| S-EPMC2882737 | biostudies-literature
Project description:Nutrient availability is an important environmental variable during development that has significant effects on the metabolism, health, and viability of an organism. To understand these interactions for the nutrient copper, we used a chemical genetic screen for zebrafish mutants sensitive to developmental copper deficiency. In this screen, we isolated two mutants that define subtleties of copper metabolism. The first contains a viable hypomorphic allele of atp7a and results in a loss of pigmentation when exposed to mild nutritional copper deficiency. This mutant displays incompletely penetrant skeletal defects affected by developmental copper availability. The second carries an inactivating mutation in the vacuolar ATPase that causes punctate melanocytes and embryonic lethality. This mutant, catastrophe, is sensitive to copper deprivation revealing overlap between ion metabolic pathways. Together, the two mutants illustrate the utility of chemical genetic screens in zebrafish to elucidate the interaction of nutrient availability and genetic polymorphisms in cellular metabolism.
| S-EPMC2576455 | biostudies-literature
Project description:In 2018, data from a surveillance study in Botswana evaluating adverse birth outcomes raised concerns that women on antiretroviral therapy (ART) containing dolutegravir (DTG) may be at increased risk for neural tube defects (NTDs). The mechanism of action for DTG involves chelation of Mg2+ ions in the active site of the viral integrase. Plasma Mg2+ homeostasis is maintained primarily through dietary intake and reabsorption in the kidneys. Inadequate dietary Mg2+ intake over several months results in slow depletion of plasma Mg2+ and chronic latent hypomagnesemia, a condition prevalent in women of reproductive age worldwide. Mg2+ is critical for normal embryonic development and neural tube closure. We hypothesized that DTG therapy might slowly deplete plasma Mg2+ and reduce the amount available to the embryo, and that mice with pre-existing hypomagnesemia due to genetic variation and/or dietary Mg2+ insufficiency at the time of conception and initiation of DTG treatment would be at increased risk for NTDs. We used two different approaches to test our hypothesis: 1) we selected mouse strains that had inherently different basal plasma Mg2+ levels and 2) placed mice on diets with different concentrations of Mg2+. Plasma and urine Mg2+ were determined prior to timed mating. Pregnant mice were treated daily with vehicle or DTG beginning on the day of conception and embryos examined for NTDs on gestational day 9.5. Plasma DTG was measured for pharmacokinetic analysis. Our results demonstrate that hypomagnesemia prior to conception, due to genetic variation and/or insufficient dietary Mg2+ intake, increases the risk for NTDs in mice exposed to DTG. We also analyzed whole-exome sequencing data from inbred mouse strains and identified 9 predicted deleterious missense variants in Fam111a that were unique to the LM/Bc strain. Human FAM111A variants are associated with hypomagnesemia and renal Mg2+ wasting. The LM/Bc strain exhibits this same phenotype and was the strain most susceptible to DTG-NTDs. Our results suggest that monitoring plasma Mg2+ levels in patients on ART regimens that include DTG, identifying other risk factors that impact Mg2+ homeostasis, and correcting deficiencies in this micronutrient might provide an effective strategy for mitigating NTD risk.
| S-EPMC10292217 | biostudies-literature
Project description:Dietary consumption of long-chain omega-3 polyunsaturated fatty acids (n-3 PUFA) may protect against cardiometabolic disease through modulation of systemic and adipose inflammation. However, it is often difficult to detect the subtle effects of n-3 PUFA on inflammatory biomarkers in traditional intervention studies. We aimed to identify novel n-3 PUFA modulated gene expression using unbiased adipose transcriptomics during evoked endotoxemia in a clinical trial of n-3 PUFA supplementation. We analyzed adipose gene expression using RNA sequencing in the fenofibrate and omega-3 fatty acid modulation of endotoxemia (FFAME) trial of healthy individuals at three timepoints: before and after n-3 PUFA supplementation (n=8; 3600mg/day EPA/DHA) for 6weeks compared with placebo (n=6), as well as during a subsequent evoked inflammatory challenge (lipopolysaccharide 0.6ng/kg i.v.). As expected, supplementation with n-3 PUFA vs. placebo alone had only modest effects on adipose tissue gene expression, e.g., increased expression of immediate early response IER2. In contrast, the transcriptomic response to evoked endotoxemia was significantly modified by n-3 PUFA supplementation, with several genes demonstrating significant n-3 PUFA gene-nutrient interactions, e.g., enhanced transcriptional responses in specific immune genes IER5L, HES1, IL1RN, CCL18, IL1RN, IL7R, IL8, CCL3 and others. These data highlight potential mechanisms whereby n-3 PUFA consumption may enhance the immune response to an inflammatory challenge. In conclusion, unbiased transcriptomics during evoked inflammation reveals novel immune modulating functions of n-3 PUFA nutritional intervention in a dynamic pathophysiological setting.
| S-EPMC4808243 | biostudies-literature
Project description:Microbial interactions affect community stability and niche spaces in all ecosystems. However, it is not clear what factors influence these interactions, leading to changes in species fitness and ecological niches. Here, we utilized 16 monocultures and their corresponding pairwise co-cultures to measure niche changes among 16 cultivable bacterial species in a wide range of carbon sources, and we used resource availability as a parameter to alter the interactions of the synthetic bacterial community. Our results suggest that metabolic similarity drives niche deformation between bacterial species. We further found that resource limitation resulted in increased microbial inhibition and more negative interactions. At high resource availability, bacteria exhibited little inhibitory potential and stronger facilitation (in 71% of cases), promoting niche expansion. Overall, our results show that metabolic similarity induces different degrees of resource competition, altering pairwise interactions within the synthetic community and potentially modulating bacterial niches. This framework may lay the basis for understanding complex niche deformation and microbial interactions as modulated by metabolic similarity and resource availability.IMPORTANCEUnderstanding the intricate dynamics of microbial interactions is crucial for unraveling the stability and ecological roles of diverse ecosystems. However, the factors driving these interactions, leading to shifts in species fitness and ecological niches, remain inadequately explored. We demonstrate that metabolic similarity serves as a key driver of niche deformation between bacterial species. Resource availability emerges as a pivotal parameter, affecting interactions within the community. Our findings reveal heightened microbial inhibition and more negative interactions under resource-limited conditions. The prevalent facilitation is observed under conditions of high resource availability, underscoring the potential for niche expansion in such contexts. These findings emphasize that metabolic similarity induces varying degrees of resource competition, thereby altering pairwise interactions within the synthetic community and potentially modulating bacterial niches. Our workflow has broad implications for understanding the roles of metabolic similarity and resource availability in microbial interactions and for designing synthetic microbial communities.
| S-EPMC10807438 | biostudies-literature