Obesity, Leptin, and the Brain

Abstract

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 . . .