Nature Neuroscience8, 566 - 570 (2005)
Published online: 26 April 2005; | doi:10.1038/nn1454
Molecular and anatomical determinants of central leptin resistance
Heike Münzberg
& Martin G Myers Jr
Heike Münzberg and Martin G. Myers, Jr. are in the Division of Metabolism, Endocrinology and Diabetes, Department of Medicine and Department of Molecular and Integrative Physiology, University of Michigan Medical School, 1150 West Medical Center Drive, Ann Arbor, Michigan 48109, USA.
Correspondence should be addressed to Martin G Myers Jr mgmyers@umich.edu
The increasing incidence of obesity in developed nations is an ever-growing challenge to health care, promoting diabetes and other diseases. The hormone leptin, which is derived from adipose tissue, regulates feeding and energy expenditure. Most forms of obesity are associated with diminished responsiveness to the appetite-suppressing effects of leptin. Here we review the mechanisms by which leptin activates intracellular signals, the roles of these signals in leptin action in vivo, and mechanisms that may attenuate leptin signaling, limiting its action in obese individuals. We highlight data regarding the expression of SOCS3 (a potential mediator of leptin resistance) in the arcuate nucleus of the hypothalamus.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
