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Narrative review uncovers neuroendocrine networks and genetic loci regulating satiety in global populations, highlighting novel therapeutic targets for obesity management.
The prevalence of obesity, which is a heritable trait that arises from the interactions of multiple genes and lifestyle factors, continues to increase worldwide, causing serious health problems and imposing a substantial economic burden on societies. For the past several years, various genetic epidemiological approaches have been utilized to identify genetic loci for obesity. Recent evidence suggests that development of obesity involves hormones and neurotransmitters (such as leptin, cocaine- and amphetamine-regulated transcript (CART), and ghrelin) that regulate appetite and energy expenditure. These hormones act on specific centers in the brain that regulate the sensations of satiety. Mutations in these hormones or their receptors can lead to obesity. Aberrant circadian rhythms and biochemical pathways in peripheral organs or tissues have also been implicated in the pathology of obesity. More interestingly, increasing evidence indicates a potential relation between obesity and central nervous system disorders (such as cognitive deficits). This paper discusses recent advances in the field of genetics of obesity with an emphasis on several established loci that influence obesity. These recently identified loci may hold the promise to substantially improve our insights into the pathophysiology of obesity and open up new therapeutic strategies to combat growing obesity epidemic facing the human population today.
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Cheung et al. (2012) studied this question.
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