4.5 Article

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

Journal

MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 232, Issue 1-2, Pages 1-8

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2005.01.006

Keywords

hyperinsulinemia; liver cirrhosis; resistin; tumor necrosis factor-alpha

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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-alpha (TNF-alpha), hyperinsulinemia and insulin resistance. The study aimed to examine resistin expression and its association with insulin and TNF-alpha 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-alpha compared to sham animals. In addition, epididymal TNF-alpha 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-alpha to cultured fat pads increased resistin gene expression significantly. These results implied that hyperinsulinemia and increased TNF-alpha 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. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

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