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

作者: Zhuowei Wang , Yan-Ting Zhou , Tetsuya Kakuma , Young Lee , Satya P Kalra

DOI: 10.1006/BBRC.2000.3615

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

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