Abstract
The deposition of excess amounts of energy in adipose tissue is enhanced by high-fat diets and lack of physical activity. Furthermore, the existence of a specific genetic predisposition towards the development of obesity becomes evident by marked interindividual differences in the response to caloric oversupply. In recent years, numerous genes and genetic defects with importance for human obesity were identified, especially through studies in animal models. The adipocyte-derived hormone leptin and its hypothalamic receptor play a premier role, as they interact with a network of proteins and neuropeptides within the regulation of food intake and energy expenditure. The search for the key molecular mechanisms in the pathogenesis of obesity will not only improve our understanding of energy metabolism, but may ultimately also lead to the development of new treatment strategies for obese patients.
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