Obesity, Leptin, and the Brain

The notion that genetic abnormalities contribute to obesity gained important support with the identification of the ob gene and its protein product in 1994.1 The ob protein, termed “leptin” from the Greek leptos, meaning thin, is produced in adipose tissue and is thought to act as an afferent satiety signal in a feedback loop that putatively affects the appetite and satiety centers of the brain. The ultimate effect of this loop is to regulate body-fat mass. In ob/ob mice, which are markedly hyperphagic and obese, the ob gene is mutated and no leptin is produced; when given leptin, they stop . . .