Title page 12: Rewrite all the books on obestiy
“For instance, the recent discoveries in genetics have found that people differ in their perceptions of hunger and satiety on a genetic basis and that predisposed subgroups of the population may be particularly vulnerable to obesity in “obesogenic” societies with unlimited access to food. This notion must lead to a more open attitude toward obese people and a reduction in discrimination against them [123], it is clear that obesity cannot be considered as a consequence only of indolence or lack of will, as often thought in our societies. In the long term, we are confident that progress in genetics will help to develop useful diagnostic and predictive tests and design new treatments.”
Curr Genomics. 2011 May;12(3):169-79.
Genetics of Obesity: What have we Learned?
Choquet H, Meyre D.
Source
Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, Emeryville, California 94608, USA.
Abstract
Candidate gene and genome-wide association studies have led to the discovery of nine loci involved in Mendelian forms of obesity and 58 loci contributing to polygenic obesity. These loci explain a small fraction of the heritability for obesity and many genes remain to be discovered. However, efforts in obesity gene identification greatly modified our understanding of this disorder. In this review, we propose an overlook of major lessons learned from 15 years of research in the field of genetics and obesity. We comment on the existence of the genetic continuum between monogenic and polygenic forms of obesity that pinpoints the role of genes involved in the central regulation of food intake and genetic predisposition to obesity. We explain how the identification of novel obesity predisposing genes has clarified unsuspected biological pathways involved in the control of energy balance that have helped to understand past human history and to explore causality in epidemiology. We provide evidence that obesity predisposing genes interact with the environment and influence the response to treatment relevant to disease prediction.
“For instance, the recent discoveries in genetics have found that people differ in their perceptions of hunger and satiety on a genetic basis and that predisposed subgroups of the population may be particularly vulnerable to obesity in “obesogenic” societies with unlimited access to food. This notion must lead to a more open attitude toward obese people and a reduction in discrimination against them [123], it is clear that obesity cannot be considered as a consequence only of indolence or lack of will, as often thought in our societies. In the long term, we are confident that progress in genetics will help to develop useful diagnostic and predictive tests and design new treatments.”
Curr Genomics. 2011 May;12(3):169-79.
Genetics of Obesity: What have we Learned?
Choquet H, Meyre D.
Source
Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, Emeryville, California 94608, USA.
Abstract
Candidate gene and genome-wide association studies have led to the discovery of nine loci involved in Mendelian forms of obesity and 58 loci contributing to polygenic obesity. These loci explain a small fraction of the heritability for obesity and many genes remain to be discovered. However, efforts in obesity gene identification greatly modified our understanding of this disorder. In this review, we propose an overlook of major lessons learned from 15 years of research in the field of genetics and obesity. We comment on the existence of the genetic continuum between monogenic and polygenic forms of obesity that pinpoints the role of genes involved in the central regulation of food intake and genetic predisposition to obesity. We explain how the identification of novel obesity predisposing genes has clarified unsuspected biological pathways involved in the control of energy balance that have helped to understand past human history and to explore causality in epidemiology. We provide evidence that obesity predisposing genes interact with the environment and influence the response to treatment relevant to disease prediction.
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