Gene By Environment Interactions Between Three Candidate Genes For Obesity And Omega 3 Polyunsaturated Fatty Acids
DOWNLOAD
Download Gene By Environment Interactions Between Three Candidate Genes For Obesity And Omega 3 Polyunsaturated Fatty Acids PDF/ePub or read online books in Mobi eBooks. Click Download or Read Online button to get Gene By Environment Interactions Between Three Candidate Genes For Obesity And Omega 3 Polyunsaturated Fatty Acids book now. This website allows unlimited access to, at the time of writing, more than 1.5 million titles, including hundreds of thousands of titles in various foreign languages. If the content not found or just blank you must refresh this page
Gene By Environment Interactions Between Three Candidate Genes For Obesity And Omega 3 Polyunsaturated Fatty Acids
DOWNLOAD
Author : Renee Leigh Pasker
language : en
Publisher:
Release Date : 2008
Gene By Environment Interactions Between Three Candidate Genes For Obesity And Omega 3 Polyunsaturated Fatty Acids written by Renee Leigh Pasker and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2008 with Yupik Eskimos categories.
"Multi-factorial diseases, like obesity, are caused by genetic and environmental factors. Few studies examine potential interactions between genetic and environmental factors. Understanding these interactions can lead to better disease prevention. One important environmental factor related to obesity is omega-3 fatty acids. Yup'ik Eskimos consume a high amount of two omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). This study examined 10 single nucleotide polymorphisms (SNPs) in three genes: ADIPOQ, PPARG, and PPARGC1A. Also, 7 obesity phenotypes were examined: BMI, percent body fat, waist circumference, sum of skin-folds, plasma adiponectin, plasma triglycerides, and HDL cholesterol. Associations between these SNPs and phenotypes in 981 related Yup'ik Eskimos were examined using mixed models. Interactions were investigated with these SNPs and ð15N, a biomarker used to determine intake of EPA and DHA. The results showed that EPA and DHA modify the expression of all three genes. Additionally, SNPs in all three genes were associated with one or more obesity phenotypes. The most statistically significant results were with two SNPs in ADIPOQ and plasma adiponectin. This study supports the role of these genes in the etiology of obesity. Finally, this study demonstrates that these genes are influenced by EPA and DHA"--Leaf iii.
Polyunsaturated Fatty Acid Metabolism
DOWNLOAD
Author : Graham C. Burdge
language : en
Publisher: Elsevier
Release Date : 2018-05-04
Polyunsaturated Fatty Acid Metabolism written by Graham C. Burdge and has been published by Elsevier this book supported file pdf, txt, epub, kindle and other format this book has been release on 2018-05-04 with Science categories.
Polyunsaturated Fatty Acid Metabolism explores a number of major roles of PUFA in the body, including its role as a component of cell membranes and how it provides substrates for the synthesis of lipid second messengers. Recent studies are unraveling the effect of interactions between diet and endocrine factors and genetic and epigenetic variation on the regulation of PUFA biosynthesis in animals. Together, these recent findings provide novel insights into the impact of differences in PUFA supply on health. This book captures these findings in a manner that marks the state-of-the-art, placing them in the wider context of PUFA metabolism and nutritional science. Users will find a comprehensive discussion on the topic that presents the contributions of leading researchers who combine their knowledge to create a cohesive academic resource for researchers, those involved in production, and health policymakers. Provides a comprehensive view of polyunsaturated fatty acid metabolism Describes underlying metabolism on lipids that include polyunsaturated fatty acids Includes discussions on recent findings on the genetic and epigenetic regulation of polyunsaturated fatty acid metabolism
Candidate Genes For Obesity And Related Phenotypes
DOWNLOAD
Author : Michael Swarbrick
language : en
Publisher:
Release Date : 2002
Candidate Genes For Obesity And Related Phenotypes written by Michael Swarbrick and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2002 with Obesity categories.
The current epidemic of obesity poses a substantial threat to public health worldwide. Obesity is associated with many deleterious health conditions, including type 2 diabetes, hypertension, dyslipidaemia, respiratory conditions, arthritis, and some forms of cancer. Moreover, the rising prevalence of obesity has been accompanied by a substantial increase in the cost of treating these conditions. Obesity results from a complex interaction between behavioural, environmental, and genetic factors. While the recent increase in the prevalence of obesity is largely due to behavioural factors (for example, physical inactivity); it has also been observed that genetic factors make a large contribution to individual susceptibility. In fact, studies indicate that as much as 50 - 80% of the variation in measures of obesity can be attributed to the effects of genes. Furthermore, closer examination of this genetic component using segregation analysis has indicated the presence of common genes for obesity, with large effects on the phenotype. However, these putative major genes for obesity have not yet been identified. The aim of this thesis was to investigate the role of three distinct genetic loci in obesity and related cardiovascular factors, including type 2 diabetes and dyslipidaemia. The aim of the first investigation was to test whether a common polymorphism (Pro12Ala) in the gene encoding peroxisome proliferator-activated receptor gamma 2 (PPAR-γ2) was associated with obesity and other cardiovascular risk factors in a large group of Caucasian subjects. PPAR-γ2 is an adipogenic transcription factor, which also regulates insulin sensitivity in adipose tissue. No association was observed between the Pro12Ala polymorphism and obesity in Caucasians, but obese subjects carrying the Ala allele displayed an altered blood lipid profile compared with obese Pro/Pro subjects. As the Pro12Ala polymorphism may exacerbate the risk of cardiovascular disease by modifying blood lipid profile in obesity, this relationship was examined further in a separate population. The aim of the second investigation was to determine whether the Pro12Ala polymorphism was associated with obesity, dyslipidaemia, diabetes and carotid intima-medial wall thickening in a population at high risk of developing cardiovascular disease. Australian Aboriginal people display high rates of mortality from cardiovascular disease, and it is possible that their increased susceptibility is due to genetic factors. However, the results from the Aboriginal population confirmed the results of the first study: there was no intrinsic association between the Pro12Ala variant and obesity. In addition, the Ala allele was not associated with deleterious changes in blood lipid profile, as it was in Caucasians. The aim of the third investigation was to confirm the presence of a quantitative trait locus (QTL) for obesity on chromosome 20q13. Highly polymorphic genetic markers in this region were tested for linkage and association with several measures of obesity in a Caucasian population. None of the measures of obesity were linked to or associated with markers spanning 20q13, suggesting that this chromosomal region does not contain a major locus for obesity in this Caucasian population. In the fourth investigation, the 5' sequence of Agouti Signalling Protein (ASIP) was identified. ASIP is a candidate gene for obesity, as it is expressed at high levels in adipocytes, and may participate in several obesity-related processes. Three new exons and two alternative promoters were identified for the ASIP gene. These results may lead to greater understanding of the role of ASIP in obesity and adipocyte metabolism; and may also be used to direct further research into genetic variation within this candidate gene. In conclusion, extensive study of two established candidate genetic loci revealed no association with measures of obesity. Therefore, it is likely that loci other than these make significant contributions to obesity in humans. Further investigation of novel candidate genes, such as ASIP, may allow the identification of novel genetic polymorphisms and new pathways important for the genetic basis of obesity.
Metabolic Effects Of Omega 3 Long Chain Polyunsaturated Fatty Acids
DOWNLOAD
Author : Benjamin B. Albert
language : en
Publisher:
Release Date : 2016
Metabolic Effects Of Omega 3 Long Chain Polyunsaturated Fatty Acids written by Benjamin B. Albert and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2016 with categories.
Obesity and its associated cardiometabolic disorders are among the world's greatest health problems. However, non-surgical weight-loss treatments are ineffective. Treatments that can reduce cardiometabolic risk in the overweight and obese are urgently needed. Further, as the offspring of obese and/or diabetic women are programmed to become obese and insulin resistant with age, interventions in pregnancy could have substantial long-term impacts on public health. Supplemental omega-3 fatty acids appear promising as they modulate important metabolic pathways and are insulin-sensitising in rats. The central hypothesis in this thesis is that long chain omega-3 polyunsaturated fatty acids, can modify the effects of gene-environment interactions to improve aspects of glucose and lipid metabolism. Four predictions were tested 1) that an n-3 PUFA supplement would be insulin sensitising in overweight men and 2) that an n-3 PUFA supplement used in a model of insulin resistant pregnancy would have metabolic benefits to the offspring 3) that fish oils sold at retail would have excessive oxidation, and 4) that an oxidised fish oil supplement would not have benefits to the offspring when used during pregnancy. I used a randomised controlled crossover trial to investigate the metabolic effects of krill/salmon blended oil on insulin sensitivity in overweight men. At baseline, higher n-3 PUFA levels were associated with greater insulin sensitivity. However, supplementation with the marine oil led to reduced insulin sensitivity, suggesting increased cardiometabolic risk. In an animal model of insulin-resistant pregnancy (maternal high-fat diet supplementation with unoxidized fish oil prevented the development of insulin resistance in the adult offspring. I found that fish oil products purchased at retail were substantially oxidised and did not meet labelled n-3 PUFA content. I then assessed the effects of oxidised fish oil supplementation during rat pregnancy, and found a substantial increase in neonatal mortality and persistent maternal insulin resistance. I have shown that oxidation changes the metabolic effects of n-3 PUFA rich supplements. It is possible that there are negative consequences to consuming oxidised fish oil during human pregnancy, and unrecognised oxidation may have confounded the n-3 PUFA clinical trial literature. Whether n-3 PUFAs have insulin-sensitising effects in humans remains unresolved
Fat Detection
DOWNLOAD
Author : Jean-Pierre Montmayeur
language : en
Publisher: CRC Press
Release Date : 2009-09-14
Fat Detection written by Jean-Pierre Montmayeur and has been published by CRC Press this book supported file pdf, txt, epub, kindle and other format this book has been release on 2009-09-14 with Medical categories.
Presents the State-of-the-Art in Fat Taste TransductionA bite of cheese, a few potato chips, a delectable piece of bacon - a small taste of high-fat foods often draws you back for more. But why are fatty foods so appealing? Why do we crave them? Fat Detection: Taste, Texture, and Post Ingestive Effects covers the many factors responsible for the se
Effects Of The Fto Gene And Environment On Obesity In European Children
DOWNLOAD
Author : Anna Christina Koni
language : en
Publisher:
Release Date : 2013
Effects Of The Fto Gene And Environment On Obesity In European Children written by Anna Christina Koni and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2013 with Obesity in children categories.
Childhood obesity is considered to be one of the most serious public health problems of the 21st century. The worldwide prevalence of obesity has increased dramatically over the past three decades and while continuing to rise at a rapid rate, along with increasing levels of childhood obesity, are having a profound effect on healthcare development in many low- and middle-income countries, particularly in urban environments. Longitudinal and cross sectional studies have indicated clear associations between environment and obesity risk. In addition, childhood obesity leads to serious health conditions such as cardiovascular disease, type II diabetes and adulthood obesity. Environmental factors, however, do not seem to explain neither all of the variance in childhood obesity prevalence, nor all the variance in response to intervention studies. Although the human genome has not changed over the years, obesity levels and mortality rates have dramatically increased, thus it becomes more evident that environmental factors such as physical activity or sedentary lifestyle may have a key role in this increase of obesity prevalence. However, since the prevalence of childhood obesity is different in certain geographical areas of the world, it is important to investigate the genetic predisposition in relation to its interaction with environmental influences. Genetic studies have demonstrated a contribution of specific genetic variants to obesity in adults. Additionally, heritability studies of childhood obesity support the idea that genetic predisposition may also be a factor in determining childhood obesity or adiposity. The obesity prevalence research becomes even more complicated by gene-environment interactions, where individuals with different genotypes respond differently in certain environments and therefore it is more challenging to define the actual causes of this health problem. The overall aim of this study was to investigate the interplay between genetic and environmental influences such as physical activity on the predisposition to childhood obesity related traits in the IDEFICS cohort. This thesis focused on European children from eight countries participating in the IDEFICS Study including Germany, Italy, Spain, Cyprus, Estonia, Sweden, Belgium and Hungary aged two to ten. The main objective was to characterize the relative contributions of individual genes, environmental factors and gene-environment interactions to this risk. In doing so, this investigation also allowed comparisons between the different age groups and countries and also possible differences between the two sexes. These findings will add to the existing efforts aimed at finding appropriate treatments and effective preventative intervention programs around Europe. In order to explore how environment and genes interact and whether genes can modulate the development of obesity in children of this European population, a detailed characterization of body composition, physical activity patterns, socio-economic, and genetic factors was performed. The main findings from this thesis were that: (a) age is an important factor when studying childhood obesity as body composition changes in a significant way with age, in both boys and girls. These findings also highlight the fact that various environmental and lifestyle effects 4 © A. C. Koni (2013) related to childhood obesity, such as physical activity (PA), differ between the two sexes and among age groups; (b) physical activity and sedentary behaviours may influence obesity related phenotypes in children of European origin. These associations persist after adjustment for a comprehensive range of potential confounding factors; (c) the Fat Mass Obesity-associated (FTO) gene influences obesity related phenotypes in children of European origin. These associations persist after adjustment for a comprehensive range of potential confounding factors; (d) although there was no Gene*PA interaction, physical activity or inactivity seems to play a role in modulating the genetic predisposition to obesity in children. The findings of this study demonstrate that there was a trend of decreased obesity risk phenotypes in children that were more physically active overall. This observation has important public health value, as the data of this thesis indicate that being physically active may have a protective role in the genetic predisposition to obesity induced by variation in the FTO gene. Further studies into the mechanisms underpinning this effect are needed in order to more effectively develop accurate design, as well as implementation strategies to reduce childhood obesity and for advancing the basic understanding of the mechanisms behind human obesity and its relationship with genetics.
The Genetic Mechanisms Underlying Human Obesity
DOWNLOAD
Author : Stephen James Clark
language : en
Publisher:
Release Date : 2013
The Genetic Mechanisms Underlying Human Obesity written by Stephen James Clark and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2013 with categories.
Obesity is becoming one the leading causes of mortality in the western world. Although environment is a factor in its development, it is highly heritable and despite a number of genes that have been found to be associated to the disease its genetics are still poorly understood. Discovery of genetic pathways that influence obesity risk can provide a better understanding of the pathophysiology of the disease and identify possible pharmacological targets for its treatment. This project was designed to investigate possible genetic associations between five candidate genes and severe obesity in both adult and child French Caucasians (n=2,822). Tag SNPs were chosen along with a selection of common SNPs not in the HapMap database and genotyped using Sequenom iPLEX assays. Putative associations were discovered to obesity in three genes, SIRT1 (corrected p-values: 0.034, 0.019), APLN (corrected p-value: 0.017) and IL11 (corrected p-value: 0.016), although associations do not withstand genome-wide correction. SIRT1 and IL11 SNPs were subsequently genotyped within a family cohort for which transcription data in adipose tissue was available. In this cohort, SIRT1 genotypes were nominally associated with BMI (corrected p-values: 0.014, 0.019, 0.014) and a significant difference in expression levels of the gene was observed between lean and obese individuals (p=1.6x10-35) providing suggestive evidence of a role of this gene in the development of obesity. Expression and genotypes of another gene, IRS1 were also analysed and although no significant associations to obesity were found, an association between SNP variation and gene expression was discovered (corrected p-value: 1.0x10-5). Another aim of this project was to investigate the possibility that DNA methylation influences obesity risk. Firstly, a method for the measurement of the quantitative trait of DNA methylation status at individual CpG sites was developed using direct sequencing. Next, methylation in the leptin gene CpG island was measured in a subset of 184 case-control samples and a nominal association was discovered between the quantitative measurement of methylation at a single CpG site and obesity (p=0.013). In summary, putative associations to obesity have been discovered with genetic variants as well as transcription levels and CpG methylation. Replication in other populations is required in order to confirm these associations.
Identification Of Direct And Indirect Genetic Effects On Obesity In Mice
DOWNLOAD
Author : Kari Haus
language : en
Publisher:
Release Date : 2010
Identification Of Direct And Indirect Genetic Effects On Obesity In Mice written by Kari Haus and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2010 with categories.
Obesity is a complex disease with both the environment and allelic variants controlling appetite and metabolism. Although rare forms of monogenic obesity have been identified in a few humans, we currently theorize that the majority of cases of overweight and obesity are due to the regulation of pathways dictating hunger and energy expenditure ill-fitted the current obesogenic environment. Research using inbred mouse strains has proved fruitful in identifying murine genetic components of these metabolic pathways that have orthologous function in humans. However, most of the studies assume that interactions between an individual's genome and the environment are causative for over-accumulation of adipose tissue. Indirect genetic effects, the effects of parental genes on gene expression and metabolic pathway development in the progeny, can also play an important role in obesity. We have performed breeding experiments designed to differentiate between direct and indirect genetic effects using subcongenics of the B6.C-Tyrc̳ H1b̳ Hbbd̳/ByJ congenic mouse strain. This strain harbors BALB/cByJ donor alleles on distal chromosome 7 in a C57BL/6ByJ background. I identified a genomic region spanning 2.8Mb in which BALB/cByJ alleles promoted obesity with direct genetic effects. While the genomic region was small, sequence and gene expression analysis revealed that four of the eight protein coding genes in the congenic donor region were candidate obesity genes. I also found two separate indirect genetic effects loci where maternal BALB/cByJ alleles acted postnatally to change the adiposity of nursing pups. These maternal effects loci behaved oppositely; one promoted leanness and the other promoted adiposity. I identified strong candidate genes for both maternal effects loci; prolylcarboxypeptidase (Prcp), family with sequence similarity 181, member b (Fam181b) and RAB30 member RAS oncogene family (Rab30) are candidate genes promoting leanness in a genomic region proximal to the obesity causing potassium channel tetramerization domain containing-14 (Kctd14). I hypothesized that postnatal maternal influences on adiposity were mediated through metabolic imprinting. Metabolic imprinting occurs during critical windows in gestational and neonatal development when imprinting is set and neuronal connections in regions of the brain controlling appetite are formed. Future work involves the characterization of genetic pathways contributing to these phenomena.
Assessment Of Gene Retail Food Environment Interactions On Diet And Obesity Related Outcomes
DOWNLOAD
Author : Yang Han
language : en
Publisher:
Release Date : 2021
Assessment Of Gene Retail Food Environment Interactions On Diet And Obesity Related Outcomes written by Yang Han and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2021 with categories.
"Background The role of the food environment in obesity risk is unclear, which may be due in part to imprecision in food environment measurements and lack of consideration of individual differences in responsivity to food cues encountered in the food environment. We aimed to assess interactions between neighbourhood in-store retail food measures and two genetic factors, polygenic risk score and DRD4 gene expression, on diet and adiposity outcomes. Methods Genetic, dietary, lifestyle, and anthropometric data were obtained from CARTaGENE biobank comprised of men and women who are representative of middle-aged adults in Quebec (n=3,718). Data from the CARTaGENE biobank were then geotemporally linked to in-store retail food marketing data based on the forward sortation area and year quarter of data collection. A ratio variable of vegetables to soft drink data was calculated for retail categories (in-store displays, price/discount, and variety) to estimate the relative healthfulness of retail exposures. Genetic risk of obesity was assessed with a 97 single nucleotide polymorphism polygenic risk score (PRS). High and low (median split) prefrontal DRD4 expression (pDRD4) was estimated using genome-wide genotyping data and the PrediXcan method. Dietary outcomes included the Canadian-adapted Healthy Eating Index 2010 and its individual components. Generalized linear models were used to evaluate main and interactive effects between retail exposures and two genetics factor (PRS and pDRD4) on dietary and anthropometric outcomes. Models were adjusted for both individual-level (age, sex, first three components of ancestry, household income, marital status, education, smoking status, physical activity, energy misreporter status, language, season of participation) and neighbourhood-level socio-demographic factors (population density, immigration rate, employment rate, high school completion).Findings A significant interaction between PRS and regular price was observed, such that the positive association between PRS and waist circumference was strengthened with increasing price of vegetables in relation to soft drinks (0.7 cm, 95% CI (0.1,1.3); p=0.0308). Male-specific interactions were observed between pDRD4 and in-store display of vegetables in relation to soft drinks. With increasing exposure (more healthful), participants with high pDRD4 had significantly higher intake of fruits and vegetables (0.41 servings/day, 95% CI (0.22, 0.59); p
Gene Environment Interactions Underlying The Developmental Origins Of Health And Disease
DOWNLOAD
Author : Brian Spencer Knight
language : en
Publisher:
Release Date : 2008
Gene Environment Interactions Underlying The Developmental Origins Of Health And Disease written by Brian Spencer Knight and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 2008 with categories.
Retrospective epidemiological studies of British cohorts have found an inverse relationship between birth size and rates of mortality from cardiovascular disease and stroke. Subsequently, further studies in humans and in animals have demonstrated that there is an inverse relationship with a combination of suboptimal prenatal and postnatal environments and the development of the metabolic syndrome (insulin resistance, hypertension, obesity and dyslipidemia). However, recently it has been reported that not all individuals exposed to these environments develop these conditions, suggesting that an individual's genotype may contribute to the eventual outcome. Phylogenetically distinct, murine strains allow the genetic dissection of complex phenotypic traits; however, to date, they have not been utilized to evaluate the gene-environment interaction underlying these inverse relationships. Thus, A/J and C57BL/6J mice were subjected to prenatal undernutrition, to model an adverse intra-uterine environment, and although prenatal undernutrition resulted in fetal growth restriction of equal magnitude, remarkable strain differences were observed. At the end of gestation C57BL/6J mice showed significant alterations in fetal organ weights (liver, kidneys and placenta) and glucocorticoids (elevation). Postnatally, C57BL/6J offspring demonstrated catch-up growth, obesity, impaired glucose tolerance, insulin resistance, increased blood pressure, liver dysfunction and altered cardiovascular function compared to strain and gender matched controls. The A/J strain was resistant to the development of prenatal and postnatal pathologies, except they also demonstrated alterations in cardiovascular function. Females of both strains displayed a more moderate phenotype than the males. Although feeding undernutrition mice an atherogenic diet postnatally did not exacerbate the phenotype, postnatal dietary supplementation of omega-3 long chain unsaturated fatty acids completely reversed the undernutrition induced altered metabolic phenotype in C57BL/6J. Microarray analysis revealed that adult A/J and C57BL/6J mice have distinct gene expression profiles, under control dietary conditions, and that this differential strain expression profile changes in adult offspring in response to prenatal undernutrition. The expression profiles predicted onset of metabolic and liver diseases within the C57BL/6J strain, clearly linking the observed phenotype to alterations in gene expression. These expression differences were also linked to inherent strain differences in the genetic code where a disproportionate number of differential expressed genes had function altering polymorphisms.