Signal Transduction Pathways for Leptin
Year: 2009
Type: article
Abstract: 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 …
Source: Diabetes
DOI: 10.2337/db08-1646
Author: Streamson Chua
Institution: Albert Einstein College of Medicine
Language: English
Subfield: Endocrine and Autonomic Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W2109532866