^*Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon.

Correspondence: Michael A. Cowley Division of Neuroscience, OHSU, 505 NW 185th Avenue, Beaverton, OR 97006. E-mail: cowleym@ohsu.edu

Received  0000; Revised  0000; Accepted  0000.

Abstract

The prevalence of obesity, and the human and economic costs of the disease, creates a need for better therapeutics and better understanding of the physiological processes that balance energy intake and energy expenditure. Leptin is the primary signal from energy stores and exerts negative feedback effects on energy intake. In common obesity, leptin loses the ability to inhibit energy intake and increase energy expenditure; this is termed leptin resistance. This review discusses the evidence in support of leptin resistance in mouse models and humans and the possible mechanisms of leptin resistance.