Abstract

Genetic defects underlying obesity in inbred mice have given hope of new possibilities for the pharmacologic treatment of obesity. Leptin (the ob gene product) and the leptin receptor are involved in the regulation of both appetite and energy expenditure in the mouse. Mutations in the ob gene that lead to overeating and decreased physical activity have been demonstrated in morbidly obese mice, and treatment with recombinant leptin has resulted in a marked weight reduction in these animals as well as normal mice. Similarly, mutations in the receptor gene result in marked obesity in some strains of mouse and rat. The pathophysiologic role of leptin and its feedback system in humans is yet only partly revealed. This article focuses on recent studies of the leptin pathway and its potential role in the treatment of obesity.

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