Article

Genetic Epidemiology of Obesity

Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, 1440 Canal Street, New Orleans, LA 70112, USA.
Epidemiologic Reviews (Impact Factor: 6.67). 02/2007; 29(1):49-61. DOI: 10.1093/epirev/mxm004
Source: PubMed

ABSTRACT

Obesity has become a global epidemic and contributes to the increasing burden of type 2 diabetes, cardiovascular disease, stroke, some types of cancer, and premature death worldwide. Obesity is highly heritable and arises from the interactions of multiple genes, environmental factors, and behavior. In this paper, the authors reviewed recent developments in genetic epidemiologic research, focusing particularly on several promising genomic regions and obesity-related genes. Gene-gene and gene-environment interactions of obesity were also discussed. Published studies were accessed through the MEDLINE database. The authors also searched the Obesity Gene Map Database (http://obesitygene.pbrc.edu/) and conducted a manual search using references cited in relevant papers. Heritabilities for obesity-related phenotypes varied from 6% to 85% among various populations. As of October 2005, 253 quantitative trait loci for obesity-related phenotypes have been localized in 61 genome-wide linkage scans, and genetic variants in 127 biologic candidate genes have been reported to be associated with obesity-related phenotypes from 426 positive findings. Gene-gene interactions were also observed in several genes, and some genes were found to influence the effect of dietary intake and physical activity on obesity-related phenotypes. Integration of genetic epidemiology with functional genomics and proteomics studies will be required to fully understand the role of genetic variants in the etiology and prevention of obesity.

    • "Genetic factors are thought to mediate individual differences in eating behavior under stress. Obesity has been found to be heritable; over 100 genes have been associated with this condition (Yang et al., 2007). It has been suggested that genes may influence obesity particularly in terms of promoting a behavioral trait to eat without hunger (Faith et al., 2006; Fisher et al., 2007). "
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    ABSTRACT: People often crave for high-caloric sweet foods when facing stress and this 'emotional eating' is a most important cause for weight gain and obesity. Eating under stress contrasts with the normally expected response of a loss of appetite, yet in spite of intensive research from neurobiological and cognitive disciplines we still do not know why stress or negative affect triggers overeating in so many of us. Since the prevalence of overweight and obesity still rises, the discovery of crucial risk factors is a most desirable goal of today's research on sub-optimal eating habits. This paper summarizes the most relevant current knowledge from the (human) literature regarding cognitive and biological vulnerabilities for stress-induced emotional eating. A (non-systematic) review of the most relevant studies reveals that most studies contemplate a rather one-directional way of focusing on either cognitive or biological factors, showing inconsistent results. The current paper elaborates and/or integrates these findings into a biological-cognitive interaction model in which a specific combination of genetic and cognitive vulnerabilities are thought to increase our bio-behavioral response to stress, critically increasing the rewarding value of pleasant foods and, hence, emotional eating. Copyright © 2015. Published by Elsevier Ltd.
    No preview · Article · Jan 2015 · Psychoneuroendocrinology
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    • "The quantitative genetic contribution to body mass index variation and hence to obesity is well established (Walley et al. 2009; Yang et al. 2007) and has been confirmed in the population used for the present study (Schousboe et al. 2003). Many obesity candidate genes have been discovered , among which the most consistent associations have been found between body weight and single nucleotide polymorphisms (SNP) in the fat mass and obesity associated FTO gene (Frayling et al. 2007; Jess et al. 2008; Kring et al. 2008), confirmed in a recent meta-analysis (Peng et al. 2011). "
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    ABSTRACT: In this paper it was investigated if any genotypic footprints from the fat mass and obesity associated (FTO) SNP could be found in 600 MHz 1 H CPMG NMR profiles of around 1,000 human plasma samples from healthy Danish twins. The problem was addressed with a combination of univariate and multivariate methods. The NMR data was substantially compressed using principal component anal-ysis or multivariate curve resolution-alternating least squares with focus on chemically meaningful feature selection reflecting the nature of chemical signals in an NMR spectrum. The possible existence of an FTO signature in the plasma samples was investigated at the subject level using supervised multivariate classification in the form of extended canonical variate analysis, classification tree modeling and Lasso (L1) regularized linear logistic regres-sion model (GLMNET). Univariate hypothesis testing of peak intensities was used to explore the genotypic effect on the plasma at the population level. The multivariate classi-fication approaches indicated poor discriminative power of the metabolic profiles whereas univariate hypothesis testing provided seven spectral regions with p \ 0.05. Applying false discovery rate control, no reliable markers could be identified, which was confirmed by test set validation. We conclude that it is very unlikely that an FTO-correlated signal can be identified in these 1 H CPMG NMR plasma metabolic profiles and speculate that high-throughput un-targeted genotype-metabolic correlations will in many cases be a difficult path to follow.
    Full-text · Article · Feb 2014 · Metabolomics
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    • "Metabolic disturbances in obesity causes a number of diseases, namely, cardiovascular diseases (hypertension, atherosclerosis, coronary heart disease), stroke, insulin-dependent diabetes, premature death, diseases of musculoskeletal system (osteochondrosis and metabolic-dystrophic arthritis), hepatobiliary disease (gallbladder dyskinesia, chronic cholecystitis, cholelithiasis) and number of tumor sites, including lung cancer, breast cancer, uterine cancer and ovarian; in women, there is a violation of ovarian-menstrual cycle dyslipidemia. Obesity reduces life expectancy by 3 to 5 and, sometimes, in severe forms, for 15 years [6,7]. "
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    ABSTRACT: Obesity becomes endemic today. Monosodium glutamate was proved as obesogenic food additive. Probiotics are discussed to impact on obesity development.Aims and objectives: The aim was to study the effects of probiotics on the development of monosodium glutamate (MSG)-induced obesity in rats. We included 45 Wistar male rats and divided into three groups (n = 15). Newborn rats of group 1 (control) received subcutaneously 8 mul/g saline. Group 2 received 3 to 4 mg/g MSG subcutaneously on the second, fourth, sixth, eighth and tenth day of life. Within 4 months after birth, rats were on a standard diet. Group 3 received an aqueous solution of probiotics mixture (2:1:1 Lactobacillus casei IMVB-7280, Bifidobacterium animalis VKL, B. animalis VKB) at the dose of 5 x 109 CFU/kg (50 mg/kg) intragastrically. Administration of probiotics was started at the age of 4 weeks just after weaning and continued for 3 months during 2-week courses. Group 2 received intragastrically 2.5 ml/kg water. Organometric and biochemical parameters in all groups of rats were analyzed over 4 months. The concentration of adiponectin was determined in serum, and leptin - in adipose tissue. Administration of MSG led to the development of obesity in rats; body weight had increased by 7.9% vs controls (p < 0.05); body length had increased by 5.4% (p < 0.05). Body mass index and Lee index and visceral fat mass had increased (p < 0.001). Under the neonatal injection of MSG, the concentration of total cholesterol, triglycerides, VLDL cholesterol and LDL cholesterol significantly increased (p < 0.001), in comparison with controls. Adipose-derived hormones changed in MSG obesity rats: adiponectin decreased by 58.8% (p < 0.01), and leptin concentration in adipose tissue had increased by 74.7% (p < 0.01). The probiotic therapy of rats from group 3 prevented obesity development. Parameters of rats treated with probiotic mixture did not differ from that in the control. The introduction of MSG to newborn rats caused the obesity in adulthood. Periodic administration of probiotic mixture to rat injected with MSG neonatally resulted in recovery of lipid metabolism and prevention of the obesity development.
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