Leptin resistance of adipocytes in obesity: Role of suppressors of cytokine signaling

Zhuowei Wang, Yan Ting Zhou, Tetsuya Kakuma, Young Lee, Satya P. Kalra, Pushpa S. Kalra, Wentong Pan, Roger H. Unger

Research output: Contribution to journalArticlepeer-review

79 Scopus citations


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. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)20-26
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Oct 14 2000
Externally publishedYes


  • Direct leptin action
  • Endocrine autosuppression
  • Leptin resistance
  • Obesity
  • SOCS

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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