Topic
Genetics of obesity
About: Genetics of obesity is a research topic. Over the lifetime, 185 publications have been published within this topic receiving 45110 citations. The topic is also known as: genetic obesity & genetic obesity (disease).
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TL;DR: The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
Abstract: The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
12,394 citations
University of Bristol1, University of Oxford2, Wellcome Trust Centre for Human Genetics3, Churchill Hospital4, National Health Service5, University of London6, University of Oulu7, Imperial College London8, National Institutes of Health9, Medical Research Council10, Wellcome Trust Sanger Institute11, Newcastle University12, Royal London Hospital13, Queen Mary University of London14, Ninewells Hospital15, University of Dundee16
TL;DR: A genome-wide search for type 2 diabetes–susceptibility genes identified a common variant in the FTO (fat mass and obesity associated) gene that predisposes to diabetes through an effect on body mass index (BMI).
Abstract: Obesity is a serious international health problem that increases the risk of several common diseases. The genetic factors predisposing to obesity are poorly understood. A genome-wide search for type 2 diabetes-susceptibility genes identified a common variant in the FTO (fat mass and obesity associated) gene that predisposes to diabetes through an effect on body mass index (BMI). An additive association of the variant with BMI was replicated in 13 cohorts with 38,759 participants. The 16% of adults who are homozygous for the risk allele weighed about 3 kilograms more and had 1.67-fold increased odds of obesity when compared with those not inheriting a risk allele. This association was observed from age 7 years upward and reflects a specific increase in fat mass.
4,184 citations
TL;DR: A genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals provide strong support for a role of the central nervous system in obesity susceptibility.
Abstract: Obesity is heritable and predisposes to many diseases To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals This analysis identifies 97 BMI-associated loci (P 20% of BMI variation Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis
3,472 citations
TL;DR: The data identify a novel signaling pathway in the mouse for body weight regulation and support a model in which the primary mechanism by which agouti induces obesity is chronic antagonism of the MC4-R.
2,979 citations
TL;DR: The severe obesity found in two severely obese children who are members of the same highly consanguineous pedigree provides the first genetic evidence that leptin is an important regulator of energy balance in humans.
Abstract: The extreme obesity of the obese (ob/ob) mouse is attributable to mutations in the gene encoding leptin, an adipocyte-specific secreted protein which has profound effects on appetite and energy expenditure We know of no equivalent evidence regarding leptin's role in the control of fat mass in humans We have examined two severely obese children who are members of the same highly consanguineous pedigree Their serum leptin levels were very low despite their markedly elevated fat mass and, in both, a homozygous frame-shift mutation involving the deletion of a single guanine nucleotide in codon 133 of the gene for leptin was found The severe obesity found in these congenitally leptin-deficient subjects provides the first genetic evidence that leptin is an important regulator of energy balance in humans
2,912 citations