Signal Transduction Pathways for Leptin
An Embarrassment of Riches
- From the Departments of Medicine and Neuroscience, Albert Einstein College of Medicine, Bronx, New York
- Corresponding author: Streamson Chua, Jr., schua{at}aecom.yu.edu
Leptin is a critical regulator of energy balance in mammals and has served as a launch point for innumerable studies examining the regulation of food intake and energy expenditure (1). At high physiological concentrations, leptin causes a decrease in food intake, an increase in energy expenditure, and a shift to increased fatty acid oxidation. These physiological shifts lead to a decrease in body weight and body fat content. Conversely, a lack of leptin leads to obesity due to hyperphagia and increased lipogenesis. In leptin signaling deficiencies, brown adipose tissue, a major thermogenic organ in small rodents, loses its thermogenic capacity due to diminished sympathetic nervous system activity. In this issue of Diabetes, Rahmouni et al. (2) present a new molecular mechanism by which leptin stimulates anorectic and thermogenic responses in rodents.
Given that most of leptin's actions with regard to energy balance occur within the central nervous system, it is currently accepted that a distributed network of leptin receptor–bearing neurons within the hypothalamus are responsible for mediating a concerted response to fluctuations of energy stores within adipose tissue (3). Leptin receptor–bearing neurons are …
