Commentary Cell Science Reviews Vol 5 No 4 ISSN 1742-8130

The Power of Fat

A recent series of experiments in wild type (WT) and adipocyte-specific JNK-1 knockout (KO) mice have demonstrated that JNK-1 deletion in adipocytes is protective against the appearance of hepatic insulin resistance and steatosis in mice fed a high fat diet. The data are consistent with the conclusion that high fat feeding induces the expression and secretion of IL-6 from adipocytes in a JNK-1 dependent manner, and that IL-6 is a required factor for the development of hepatic insulin resistance via induction of SOCS3 which inhibits insulin signal transduction. It is surprising that JNK-1 deletion prevented secretion of IL-6 but no other measured adipokine, and that this one factor was singularly necessary for the appearance of hepatic insulin resistance. However, the experiments were well controlled, and exogenous replacement of IL-6 in the KO mice restored the ability of high fat diet to adversely affect liver metabolism. The data do not rule out the possibility that IL-6 must act in concert with other adipokines to produce insulin resistance and steatosis in the liver. The experiments generally support the central role of adipocytes and secreted adipokines in the pathogenesis of the Metabolic Syndrome trait cluster.

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