Abstract
Obesity results from an imbalance between caloric intake and energy expenditure. Twin, adoption, and family studies have not only shown that genetic factors play an important role in the pathogenesis of obesity, but also contribute to several comorbidities including hypertension and type 2 diabetes. In recent years, several single-gene defects responsible for obesity in rodents and, in rare cases, of human obesity have been identified. Besides leptin as the most notable example, numerous other proteins and neuropeptides have recently been found that participate in a complex network to regulate food intake and energy expenditure. Interestingly, some of these molecules may also play a role in the development of obesity-related hypertension. The ongoing search for relevant genetic variants should result in a better understanding of energy metabolism and hopefully clarify molecular mechanisms underlying the association between obesity and related comorbidities. This knowledge should help develop new strategies for the treatment of obesity and associated risk factors for hypertension and related cardiovascular disorders.
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