Obesity

Gene environment interactions in obesity and pregnancy: Overweight and obesity in pregnancy: their impact on epigenetics

Nature reviews Genetics. Contact us Submission enquiries: bmcmedicalgenomics biomedcentral.

Znd are five key messages for clinicians to give to women of childbearing age that could help improve their health and the health of their children, and limit the current epidemic of obesity: Strive for a healthy weight before pregnancy. Further studies by Li et al. Cell Death Differ. This study was conducted in accordance with the principles expressed in the Declaration of Helsinki. DS and FT-A wrote the draft manuscript. GRS TG 2and postprandial triglyceride concentrations vs.

  • Inactivation of the Fto gene protects from obesity. Ethics declarations Conflict of interest The author declares no competing interests.

  • Looking from a different perspective, nutrigenetic studies also assess whether genetic factors modify the effects of specific dietary factors on diseases or related traits. Several studies have demonstrated enhanced power for large-scale association studies where the true underlying GEI model is unknown [ 3536 ].

  • A compendium of human genes regulating feeding behavior and body weight, its functional characterization and identification of GWAS genes involved in brain-specific PPI network.

  • Full size table. Kraftet al.

  • Anderson, G. A Common Variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.

REVIEW article

European journal of nutrition. These results need to be validated in further studies. Archives of general psychiatry. Obesity is associated with increased risk of chronic diseases and decreased health-related quality of life and overall life expectancy [ 2 ].

Full size table. Publication bias may have contributed to the absence of replication reports. Therefore, it is critical for researchers to conduct replication studies and to publish both positive and negative results [ 39 ]. Human heredity. Publication types Research Support, N. For FTO variant rs, a high-protein diet was found to facilitate weight loss and improvement of body composition in individuals with the risk allele of the FTO variant rs, but not in other genotypes [ 24 ].

Cytosine methylation can be mitotically inherited; thus, DNA methylation is considered a mechanism of somatic inheritance. Diabetes 57, 95— J Hepatol. Niemiec, P.

Associated Data

These findings were supported by results from IPA analysis of the top genes with nominal interactions. The marked rise in obesity observed over the last three decades suggests that behavioural and environmental factors underpin the chronic mismatch between energy intake and energy expenditure. Background: Obesity and diabetes are potentially alterable risk factors for pancreatic cancer. Both gene-and pathway-based analytic approaches have been used to integrate prior biological knowledge into association and interaction analyses [ 30 ], by combining associations of genetic variants in the same gene or biological pathway.

  • Predicting preschooler obesity at birth: the role of maternal obesity in early pregnancy. The current article gives an overview of pathophysiological changes associated with maternal obesity and their consequences on placental structure and function.

  • Objectives: Modern technology may have desensitised the 'biological clock' to environmental cues, disrupting the appropriate co-ordination of metabolic processes. Recent genome-wide association studies have identified several genes convincingly related to obesity risk, including the fat mass and obesity associated gene and the melanocortin-4 receptor gene.

  • Much insight in this regard comes from animal studies.

Obesity in pregnancy: prevalence and metabolic consequences. International Journal of Obesity Obesity triggers: sequencing the genome versus sequencing the environment. Family-based genetic studies had identified 23 genes associated with PD, having diverse functions as deficiency of synaptic transmission, vesicular recycling, lysosomal dysfunction, mitophagy.

Obesity is associated with neurodegenerative diseases Alzheimer, Parkinson, and Huntington diseases and with neurodevelopmental diseases autism disorder, schizophrenia, and fragile X envuronment. However, in spite of high leptin levels during obesity, a failure in the essential leptin mechanisms reduction in feeding behavior and increased energy expenditure is present Frederich et al. Genetic and epigenetic catalysts in early-life programming of adult cardiometabolic disorders. Furthermore, a short excurse is given on epigenetic mechanisms and emerging data regarding a putative interaction between metabolism and epigenetics.

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Further investment in studies easy ab workouts for obese with fast results GEI for obesity holds promise on several grounds [ 39 ]. In epidemiology, interaction is defined by estimating whether the degree of risk attributable to the joint effects of a genotype and an environmental factor on an outcome is greater or less than would be expected if these joint effects were additive [ 12 ]. It covers both nutrigenomics and nutrigenetics. Contact us Submission enquiries: bmcmedicalgenomics biomedcentral. Better understanding of the interplay between genetic and environmental factors is the basis for developing effective personalized obesity prevention and management strategies.

Download citation. There has been considerable progress in our understanding of the role of both genetic and environment factors in the development of obesity. This gene environment interactions in obesity and pregnancy suggested that high carbohydrate consumption was associated with an increased risk of obesity only among women with the Glu27 allele OR 2. In the near future, individuals may be able to obtain their comprehensive genetic information and thus a knowledge of their genetic predisposition to obesity and other chronic diseases. Obesity reviews : an official journal of the International Association for the Study of Obesity. References 1. The number of overweight and obese adults has been estimated to be 1.

Jiao et al. Candidate gene variants for polygenic obesity appear to disrupt pathways involved in the regulation of energy intake and expenditure and include adrenergic receptors, uncoupling proteins, PPARG, POMC, MC4R and a set of single nucleotide polymorphisms in the FTO locus. Gov't Review. The Preventing Overweight Using Novel Dietary Strategies Trial is the largest and longest-term 2-years randomized intervention trial comparing the effects of four weight-loss diets of varying macronutrient compositions [ 22 ].

Obesity during pregnancy

Deepika Shrestha1 Mohammad L. Obesity, insulin resistance, and pregnancy outcome. Mailly, F.

Park, M. Caruso, C. The study addressed whether the environment may offset genetic effects on body mass. Caloric beverages were major sources of energy among children and adults in Mexico, — However, APOE4 was associated with higher fasting glucose and insulin levels, as well as an increased metabolic syndrome risk with younger age onset Torres-Perez et al. Consequently, dysfunction and inflammation of the adipose tissue trigger impaired insulin signaling, altered secretion of adipokines and cytokines, compromised triglyceride storage, and liberation of free fatty acids.

Several approaches to assessing genome-wide environment interaction GWEI have been developed recently. This finding suggested that high carbohydrate consumption was associated with an increased risk of obesity only among women with the Glu27 allele OR obesify. Gene variants involved in pathways regulating addiction and reward behaviours may also play a role in predisposition to obesity. Progress in lipid research. Some individuals defend easily against a propensity to accumulate fat mass and become overweight whilst others are predisposed to gain weight, possibly as a function of genotype. The number of overweight and obese adults has been estimated to be 1. The New England journal of medicine.

Introduction

This modular approach is computationally straightforward. Search all BMC articles Search. The GWAS approach has made impressive progress in identifying common obesity genetic variants.

Epidemiological studies have documented that increased intakes of energy and reduced consumption of high-fiber foods, as well as sedentary lifestyle, were among the major driving forces for the epidemic of obesity. Easy ab workouts for obese with fast results The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Abstract Objectives: Modern technology may have desensitised the 'biological clock' to environmental cues, disrupting the appropriate co-ordination of metabolic processes. The GWAS approach has made impressive progress in identifying common obesity genetic variants. Volume 8 Supplement 1. Further investment in studies of GEI for obesity holds promise on several grounds [ 39 ]. Hu FB: Obesity epidemiology.

Contact us Submission enquiries: bmcmedicalgenomics biomedcentral. In the combined analysis, the differences in BMI per 10 pregnsncy alleles were 1. The Journal of nutrition. Reprints and Permissions. Progress in lipid research. The risk allele carriers consuming more than We hypothesised that increased sleep duration will offset susceptible genetic effects, resulting in reduced obesity risk.

MeSH terms

Obesity is associated with increased risk of chronic diseases and decreased health-related quality of life and overall life expectancy [ 2 ]. Publication types Research Support, Non-U. It was demonstrated that two-step approach reduced the number of SNPs tested for interactions and substantially improved the power of GWEI. Contact us Submission enquiries: bmcmedicalgenomics biomedcentral.

BMC Genet. Commonly used approaches in this regard estimate global methylation by measuring DNA methylation of surrogates such as LINE-1 or Alu elements or by employing mass spectrometry for envvironment quantification of global DNA methylation and hydroxymethylation. Although these data suggest that treatment of gestational diabetes could lower the risk of childhood obesity, a more recent study of 4- to 5-year-old children whose mothers participated in a gestational diabetes treatment trial found no difference in obesity rates between children of women who received treatment for mild gestational diabetes and children of women who did not. Willer, C. Individual variants are studied to simplify the understanding of the interaction between gene—environment. Novel candidate genes and variants underlying autosomal recessive neurodevelopmental disorders with intellectual disability.

Abstract The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Article PubMed Google Scholar. Methods: We recruited male: ; female: European children born to participants in the New Zealand centre of the International Screening for Pregnancy Endpoints sleep study. Simulation studies have demonstrated that in GEI studies, even a modest amount of measurement errors in assessing environmental exposure can result in a substantial reduction in statistical power to detect an interaction [ 40 ]. Ten genes directly involved in the circadian rhythm machinery and a further 20 genes hypothesised to be driven by cyclic oscillations were evaluated by Sequenom assay.

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Concern is rising over the rapid increases in childhood obesity and metabolic disease that will translate into later adult obesity. A case-only study. None of the individual genes or single-nucleotide polymorphism SNP except one SNP remained significant after adjusting for multiple testing.

Clinical trials Randomized controlled trial RCT is widely considered to be the most reliable design because of the randomized allocation of the exposures. This paper will discuss the various animal models of maternal overnutrition and their importance in our understanding of the mechanisms underlying altered obesity risk in offspring. This finding suggested that high carbohydrate consumption was associated with an increased risk of obesity only among women with the Glu27 allele OR 2. Abstract Obesity is a global and growing problem.

The classic prospective cohort study follows subjects over time, comparing the outcome of interest in individuals who are exposed or not exposed at baseline [ 5 ]. The number of overweight and obese adults has been estimated to be 1. In population-based case-control studies, incident or prevalent cases in the studied population are ascertained over a certain time period, while the controls are randomly selected from the same source population. However, preliminary results regarding GEI on obesity are for the most part inconclusive. Clinical trials Randomized controlled trial RCT is widely considered to be the most reliable design because of the randomized allocation of the exposures.

Toxic Food Environment

Shared genetic loci between body mass index and major psychiatric disorders. Sibling and parent-offspring correlation estimation with variable family size. Of note, analyzing siblings enabled better control of family characteristics that could confound the results.

Crit Rev Food Sci Nutr. The smaller genetic effect size at the lower post-treatment than higher pre-treatment average envvironment concentration requires that the trajectories of triglyceride reductions cannot move in parallel for different genotypes when triglycerides are decreased pharmacologically. Brisson et al. Locke, A. Epigenetic mechanisms regulate the accessibility of DNA for transcription factor complexes, the efficiency of gene transcription, and the stability of messenger RNA mRNA.

The difference between the R-carriers and GG homozygotes was seven-fold greater in obese than lean subjects 0. Current Atherosclerosis Reports Show results from All journals This journal. Exp Biol Med Maywood. Humphries, S.

Introduction

Garenc, C. Interactionss, reduced hypothalamic neurogenesis could play a role in obesity and severe hyperphagia Gray et al. A poor eating self-regulation in children has been associated with higher body weight Hughes and Frazier-Wood, Mohammad L. Furthermore, an association was found between the observed epigenetic modifications and hypertension, insulin resistance, and hyperlipidemia in the offspring [ 60 ].

Williams View author publications. Neuronal loss leads to neurodegeneration due to accumulation of eenvironment proteins in the brain. Risk prediction of prevalent diabetes in a Swiss population using a weighted genetic score-the CoLaus Study. Six new loci associated with body mass index highlight a neuronal influence on body weight regulation. Rogers I. Ball, N.

  • Roodveldt, C. Results of different models consistently revealed that the association between carrying an obesity risk variant in FTO and having a high BMI is predominantly found among individuals heavier at birth.

  • Ten genes directly involved in the circadian rhythm machinery and a further 20 genes hypothesised to be driven by cyclic oscillations were evaluated by Sequenom assay. Further confirmatory studies are required in other population cohorts of different age groups.

  • Our findings further suggest that children born smaller consequent to higher BMI GRS are very likely to experience stronger adiposity rebound effects because of compensatory catch-up growth following smaller birth size as well as increased adiposity rebound effects of the birthweight-lowering BMI loci. Dunn, A.

  • J Am Coll Nutr. Polygenic variants have a modest effect.

Download PDF. Data presented by Vohl et al. PLoS Genet. Santos-Cortez, R.

The epidemic of obesity has become a major public health problem. Aand to studying GEI a Study designs for testing GEI Over the past two decades, various study designs such as prospective cohort studies, case-control studies, case-only studies, randomized intervention trials, and twin studies have been used to test GEI [ 12 ]. The second step uses an unbiased traditional GEI test of the SNPs that passed the screening step to ensure an overall valid procedure. SBERIA first selects markers with relatively strong correlation signals, and then a weighted sum of the selected marker interaction terms is computed, where the weight corresponds to the magnitude and direction of the correlations among the markers.

Publication types

Second, inadequate statistical power due to modest sample sizes and measurement errors for environmental factors continue to be major factors interactions progress in the field [ 39 ]. Improvement in metabolic markers secondary to weight loss was greater in FTO rs A allele carriers with a low-fat hypocaloric diet [ 26 ]. The risk allele carriers consuming more than Findings to date indicate that behavioral changes such as improving diet and physical activity can substantially offset obesogenic effects of risk alleles, which has much broader clinical and public health implications. European journal of human genetics : EJHG.

  • Lee, J.

  • Several randomized dietary intervention trials of weight loss have been analyzed to provide unique insights into individualized dietary response to weight loss diets based on specific genetic variants Table 1.

  • Spaccapelo, L.

  • This article reviews recent advances in identifying gene-environment interactions related to obesity and describes epidemiological designs and newly developed statistical approaches to characterizing and discovering gene-environment interactions on obesity risk. Full size table.

With respect to lower energy expenditure, a sedentary lifestyle, or physical inactivity, due to prolonged watching TV hours, interacts with the genetic predisposition causing the development of obesity Qi et al. Child Nutr. However, average triglyceride concentrations decreased with increasing physical activity: from 1. Carmena, R. Diabetes Care. Administration of exogenous DA in ex vivo neurons induced CART expression and showed protection against brain damage by reducing inflammation activation Lin et al.

The British journal of nutrition. Publication types Research Support, Non-U. Journal of obesity. In epidemiology, interaction is defined by estimating whether the pregnwncy of risk attributable to the joint effects of a genotype and an environmental factor on an outcome is greater or less than would be expected if these joint effects were additive [ 12 ]. Gene variants involved in pathways regulating addiction and reward behaviours may also play a role in predisposition to obesity. The epidemic of obesity has become a major public health problem.

Ahmad et al. Reviewed by: Tesfaye B. Figure 6E presents Lin et al. A de novo mutation affecting human TrkB associated with severe obesity and developmental delay. References 1.

Childhood Obesity

Fast results Rev Public Health. The figure shows that h 2 increased from 0. The present study was performed to test for associations between genetic susceptibility to adulthood obesity and birthweight using genome-wide SNPs data from an African ancestry population collected in the Hyperglycemia Adverse Pregnancy Outcome HAPO study. Of these layers, we will briefly describe parent feeding behavior and food diet as part of the energy intake, an important arm of the energy balance. Genetic and environmental influences on factors associated with cardiovascular disease and the metabolic syndrome.

Looking from a different perspective, nutrigenetic studies also assess whether genetic factors modify the effects of specific dietary factors on diseases or related traits. Genetic epidemiology. Franks PW, Nettleton JA: Interwctions commentary: Gene X lifestyle interactions and complex disease traits--inferring cause and effect from observational data, sine qua non. Google Scholar. Epidemiological studies have documented that increased intakes of energy and reduced consumption of high-fiber foods, as well as sedentary lifestyle, were among the major driving forces for the epidemic of obesity. Therefore, it is critical for researchers to conduct replication studies and to publish both positive and negative results [ 39 ].

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PLoS One. The study revealed three key findings. An investigation of coronary heart disease in families. Claussnitzer, M. Plasminogen activator inhibitor-1 and the circadian clock in metabolic disorders.

  • Bahrami, S.

  • However, preliminary results regarding GEI on obesity are for the most part inconclusive.

  • Mutch, D. Brain—

  • Gene by smoking interaction: evidence for effects on low-density lipoprotein size and plasma levels of triglyceride and high-density lipoprotein cholesterol.

Google Scholar. Simulation studies have demonstrated that in GEI studies, even a modest ane of measurement errors in assessing environmental exposure can result in a substantial reduction in statistical power to detect an interaction [ 40 ]. The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Despite some progress in characterizing GEI underlying obesity, many challenges remain. In population-based case-control studies, incident or prevalent cases in the studied population are ascertained over a certain time period, while the controls are randomly selected from the same source population. Continued challenges Despite some progress in characterizing GEI underlying obesity, many challenges remain.

Given the limited number pregnxncy SNPs that are eventually tested for interactions, this approach has enhanced power over traditional methods. In the combined analysis, the differences in BMI per 10 risk alleles were 1. This design is based on the assumption that genotypes and environmental exposures are independent of each other, so that the exposures should not differ among different genotypes. The classic prospective cohort study follows subjects over time, comparing the outcome of interest in individuals who are exposed or not exposed at baseline [ 5 ].

Obesity in pregnancy: implications for the mother and lifelong health of the child. Acta— Obesity is a multifactorial and polygenic disease in which variants of different genes are associated with this disease and with the development of NDgD and NDvD Arnoldussen et al.

Obesity has become environmwnt major public health concern. We hypothesised that increased sleep duration will offset susceptible genetic effects, resulting in reduced obesity risk. The number of overweight and obese adults has been estimated to be 1. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications.

Article PubMed Google Scholar The number of overweight and obese adults has been estimated to be 1. Some individuals defend easily against a propensity to accumulate fat mass and become overweight whilst others are predisposed to gain weight, possibly as a function of genotype. Pare et al. This article reviews recent advances in identifying the genetic and environmental risk factors lifestyle and diet for obesity.

In this section, we will briefly describe the genes involved in this pathway and that have been associated with monogenic obesity, as well as their effect in developing NDgD and NDvD Table 1. Leptin plasma levels are highly correlated to IR, adipocyte number, and fat mass Friedman and Halaas, Olsen, N. The HAPO study was an observational study that enrolled over 25, pregnant women from nine countries designed to examine the association between gestational hyperglycemia and newborn outcomes.

This study demonstrated that higher education levels correlate with a lower BMI Kim, Quantile-dependent expressivity would attribute the difference to the smaller genotype differences after weight loss than before CC vs. No votes so far! Ali et al. The developmental origins of adult disease.

It covers both nutrigenomics and nutrigenetics. Further investment in studies of GEI for obesity holds promise on several grounds [ 39 ]. Gene environment interactions in obesity and pregnancy nested case-control study within a large prospective cohort can improve efficiency and reduce cost [ 20 ]. European journal of nutrition. These findings suggest that sedentary lifestyle may enhance the predisposition to elevated adiposity, whereas greater leisure time physical activity may mitigate the genetic association [ 21 ]. These findings suggested that the genetic association with adiposity was strengthened with higher consumption of fried foods. A case-only study.

  • Body composition changes induced by chronic ethanol abuse: evaluation by dual energy x-ray absorptiometry. A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance.

  • You can also search for this author in PubMed Google Scholar. Because exposure is assessed before the outcome, the cohort design is less susceptible to selection bias and differential recall bias between cases and noncases when compared to a case-control design.

  • Polygenic risk for hypertriglyceridemia is attenuated in Japanese men with high fitness levels. Non-canonical functions of the DNA methylome in gene regulation.

Some individuals defend easily against a propensity to accumulate fat mass and become overweight whilst others are predisposed to gain weight, possibly as a function of genotype. Future perspective of GEI on obesity There has been considerable progress in our understanding of the role of both genetic and environment factors in the development of obesity. For example, Qi et al. Obesity results from a complex interplay of many genetic factors and environmental factors [ 4 — 8 ]. Further investment in studies of GEI for obesity holds promise on several grounds [ 39 ]. Contact us Submission enquiries: bmcmedicalgenomics biomedcentral.

Niemiec et al. Growing into obesity: patterns of height growth in those who become normal weight, overweight, or obese as young adults. Expert Rev. Ushkaryov, Y. Published studies investigating association of adult obesity GRS with birthweight were carried out using only fetal genotypes.

Statistical and biological gene-lifestyle interactions of MC4R and Genw with diet and physical activity on obesity: new effects on alcohol consumption. Causal effects of socioeconomic status on central adiposity risks: evidence using panel data from urban Mexico. Obesity, physical inactivity, high-carbohydrate diets, alcohol intake, smoking, pregnancy, and type 2 diabetes mellitus T2DM all increase triglyceride concentrations 1.

Replication and extension of genome-wide association study results for obesity in adults from northern Sweden. In addition, a human compendium of genes associated with body weight and food intake and expressed in the brain was published by collecting data from several GWAS and some candidate genes Ignatieva et al. Early-life risk factors for dementia and cognitive impairment in later life: a systematic review and meta-analysis. Sex and gender differences in developmental programming of metabolism.

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Individual variants are studied to simplify the understanding of the interaction between gene—environment. Caruso, C. Moreover, the effect of genetic risk on BMI has been found to be higher among people exposed to obesity-precipitating environments and among African ancestry than European ancestry populations Walter et al. The GCKR ProLeu polymorphism rs affects triglyceride concentrations by increasing hepatic glucokinase activity Ghavami, A. It was shown that maternal obesity before pregnancy was associated with the methylation of CpGs in female offspring and only CpGs in male offspring.

Impact of genes and environment on obesity and cardiovascular disease. Autosomal recessive causes likely in early-onset Alzheimer disease. Ghavami, A. Author information Article notes Copyright and License information Disclaimer. Muller, L.

Future perspective of GEI on obesity There has been considerable progress in our interactions of the role of both genetic and environment factors in the development of obesity. In recent years, several cohort studies have investigated the GEI on obesity. It was demonstrated that the proposed cocktail methods did not inflate the type I error and had enhanced power under a wide range of situations [ 33 ]. Obesity is associated with increased risk of chronic diseases and decreased health-related quality of life and overall life expectancy [ 2 ]. Although recent genome-wide association studies have identified many loci related to obesity or body mass index, the identified variants explain only a small proportion of the heritability of obesity. Cite this article Huang, T. This article reviews recent advances in identifying gene-environment interactions related to obesity and describes epidemiological designs and newly developed statistical approaches to characterizing and discovering gene-environment interactions on obesity risk.

Publication types Research Support, N. It was demonstrated that the proposed cocktail methods did not inflate the type I error and had enhanced power under a wide range of situations [ 33 ]. This definition is quite helpful in the context of intervention studies where the environmental exposures can be intervened upon, such as diet and physical activity, to offset genetic risk [ 13 — 15 ]. These approaches also have the potential to identify novel SNPs that are not detected in genome wide scan.

Clinical trials Randomized controlled trial RCT is widely considered gene environment interactions in obesity and pregnancy be the most reliable design because of the randomized allocation of the exposures. Methods: Using genome-wide association studies GWAS genotype and risk factor data from the Pancreatic Cancer Case Control Consortium, we conducted a discovery study of 2, cases and 2, controls to examine gene-obesity and gene-diabetes interactions in relation to pancreatic cancer risk by using the likelihood-ratio test nested in logistic regression models and Ingenuity Pathway Analysis IPA. These approaches also have the potential to identify novel SNPs that are not detected in genome wide scan. It covers both nutrigenomics and nutrigenetics. The marked rise in obesity observed over the last three decades suggests that behavioural and environmental factors underpin the chronic mismatch between energy intake and energy expenditure.

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Biological, clinical and population relevance of 95 loci prwgnancy blood lipids. Wu, Y. In the study of gene-specific and genome-wide DNA methylation, DNA methylation is mainly studied in promoter regions of genes that are rich in CpG sites. Genetics of schizophrenia: overview of methods, findings and limitations. Figure 6B presents Yamasaki et al.

In this approach, the variance of a quantitative trait by genotypes in the presence envirronment an interaction effect was calculated, and then Levene's test was used to test if subgroup samples have equal variances. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications. A similar interaction between regular consumption of fried food and GRS in relation to obesity was observed among these three cohorts [ 6 ]. Wei et al. The genetic contribution to obesity is well established. Case-only studies can be used if the interest is limited to GEI, because the case-only design has the practical advantage that there is no need to collect control samples.

In contrast, the genetic association with BMI was weakened with increased levels of physical activity. Publication types Research Support, N. For example, Qi et al.

Google Scholar obesity and pregnancy Background: Obesity and diabetes are potentially alterable risk factors for pancreatic cancer. However, RCT is often infeasible to test the long-term effects of dietary exposures on obesity or obesity-related chronic diseases due to cost and logistic considerations. Published : 15 January Full size table. Cite this article Huang, T. The mechanisms that link maternal obesity to obesity in offspring and the level of gene-environment interactions are not well understood, but the early life environment may represent a critical window for which intervention strategies could be developed to curb the current obesity epidemic.

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Supporting this finding, Masuyama et al. Genetic and functional characterization of PCSK1. The high levels of free fatty acids contribute to insulin resistance IR Schneeberger et al. Next-generation genotype imputation service and methods. On the other hand, SCZ patients showed higher levels of Negr1 in the dorsolateral prefrontal cortex Karis et al. Triglyceride response to an intensive lifestyle intervention is enhanced in carriers of the GCKR ProLeu polymorphism.

Adult Obesity and Socioeconomic Status. Nat Rev Genet. Obesity, insulin resistance, and pregnancy outcome. Gene—obesogenic environment interactions in the UK Biobank study. The biological processes that link lower birthweight with rapid post-natal catch-up growth, early-onset adiposity rebound i. Finally, the results were pooled to produce inferential results. Ma et al.

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