Stimulated resistin expression in white adipose of rats with bile duct ligation-induced liver cirrhosis: Relationship to cirrhotic hyperinsulinemia and increased tumor necrosis factor-alpha

  • Lin S
  • Sheu W
  • Chen W
 et al. 
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Abstract

Resistin, an adipose-derived polypeptide hormone, is proposed as a candidate of insulin resistance, although its roles in inhibiting adipogenesis and in inflammation have also been suggested. Liver cirrhosis is characterized by elevated circulating proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), hyperinsulinemia and insulin resistance. The study aimed to examine resistin expression and its association with insulin and TNF-α in a cirrhotic rat model using bile duct ligation (BDL). The BDL-induced cirrhotic rats showed significantly lower fat mass, insulin sensitivity and elevated plasma insulin and TNF-α compared to sham animals. In addition, epididymal TNF-α and resistin mRNA and protein levels were higher in cirrhotic rats. In normal control rats, in vivo insulin infusion and ex vivo administration of TNF-α to cultured fat pads increased resistin gene expression significantly. These results implied that hyperinsulinemia and increased TNF-α levels might upregulate adipose resistin gene in BDL-induced liver cirrhosis. Further study is necessary to document the role of resistin in metabolic abnormalities of liver cirrhosis. © 2005 Elsevier Ireland Ltd. All rights reserved.

Author-supplied keywords

  • Hyperinsulinemia
  • Liver cirrhosis
  • Resistin
  • Tumor necrosis factor-α

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