|Qian, Hao - LINCO RESEARCH INC.|
|Compton, Mark - UNIV. OF GEORGIA|
|Hartzell, Diane - UNIV. OF GEORGIA|
|Azain, Michael - UNIV. OF GEORGIA|
|Della-Fera, Mary - UNIV. OF GEORGIA|
|Baile, Clifton - UNIV. OF GEORGIA|
Submitted to: Transworld Research Network
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 1, 2002
Publication Date: March 1, 2002
Citation: Qian, H., Compton, M.M., Hartzell, D.L., Hausman, G.J., Azain, M.J., Della-Fera, M.A., Baile, C.A. Effects of intracerebroventricular leptin administration on gene transcription in adipose tissue. 2002. v. 3. p. 249-259. Interpretive Summary: The recently discovered protein, leptin, secreted by fat cells in response to changes in body weight or energy, regulates metabolism, and fat cell function. Leptin may serve as a signal linking the body's energy regulating system with fat cell function. This is the first report to demonstrate that administration of leptin, altered fat cell function which resulted in a reduction in fat cell number. Therefore, understanding the interaction of leptin with fat cell function is necessary in order to develop new methods to optimize carcass composition.
Technical Abstract: To determine the molecular mechanism of leptin-induced apoptosis in adipose tissue, RNA levels of several genes involved in cell proliferation, differentiation and(or) apoptosis were measured. Rats received ICV injections of vehicle or 5 mcg of leptin per day. Feed restricted controls had decreased white adipose tissue levels of proliferator-activated receptor-gamma (PPAR-gamma), protein kinase C (PKC) and retinoid-X receptor (RXR) mRNA, and increased mitogen-activated protein kinase (MAPK) mRNA levels, compared to ad lib fed controls. In contrast, leptin treatment increased PPAR-gamma, RXR, nuclear factor(NF-kB) and uncoupling protein-2 (UCP2) mRNA levels. These data suggest that PPAR-gamma, RXR, NF-kB and UCP-2 are involved in leptin-induced adipose apoptosis.