Leptin resistance of adipocytes in obesity: role of suppressors of cytokine signaling.

Authors: Wang, Z  Zhou, YT  Kakuma, T  Lee, Y  Kalra, SP  Kalra, PS  Pan, W  Unger, RH 
Citation: Wang Z, etal., Biochem Biophys Res Commun. 2000 Oct 14;277(1):20-6.
Pubmed: (View Article at PubMed) PMID:11027633
DOI: Full-text: DOI:10.1006/bbrc.2000.3615

Liver-derived hyperleptinemia induced in normal rats by adenovirus-induced gene transfer causes rapid disappearance of body fat, whereas the endogenous adipocyte-derived hyperleptinemia of obesity does not. Here we induce liver-derived hyperleptinemia in rats with adipocyte-derived hyperleptinemia of acquired obesity caused by ventromedial hypothalamus lesioning (VMH rats) or by feeding 60% fat (DIO rats). Liver-derived hyperleptinemia in obese rats caused only a 5-7% loss of body weight, compared to a 13% loss in normoleptinemic lean animals; but in actual grams of weight lost there was no significant difference between obese and lean groups, suggesting that a subset of cells remain leptin-sensitive in obesity. mRNA and protein of a putative leptin-resistance factor, suppressor of cytokine signaling (SOCS)-1 or -3, were both increased in white adipose tissues (WAT) of VMH and DIO rats. Since transgenic overexpression of SOCS-3 in islets reduced the lipopenic effect of leptin by 75%, we conclude that the increased expression of SOCS-1 and -3 in WAT of rats with acquired obesity could have blocked leptin's lipopenic action in the leptin-resistant WAT population.

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CRRD Object Information
CRRD ID: 2298920
Created: 2008-07-31
Species: All species
Last Modified: 2008-07-31
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.