Abstract
Summary The recent demonstration of genetic defects underlying obesity in inbred mice has raised hopes of treating obesity pharmacologically. The obese (ob) gene, its product leptin 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 and in normal mice. The pathophysiological role of leptin and its feedback system in man is as yet only partly known. This article focuses on recent data on the ob gene pathway and its potential role in man.
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