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Transplantation Proceedings
Year: 2008  |  Volume: 40  |  Issue: 10  |  Page No.: 3330 - 3334

Hepatic Ischemia-Reperfusion Induces Insulin Resistance via Down-Regulation During the Early Steps in Insulin Signaling in Rats

C. Liu, X. Wang, Z. Chen, L. Zhang, Y. Wu and Y. Zhang    

Abstract:

Background: The effects of hepatic ischemia-reperfusion (I/R) on insulin signaling remain unclear. We observed changes in insulin secretion and signal protein expression during the early steps in insulin signaling after hepatic I/R in rats.

Materials and Methods: Eighty healthy Wistar rats were randomly divided into an I/R group and a control (C) group. After we exposed the hepatic hilum, ischemia was induced by clamping the hepatic artery and portal vein for 30 minutes and then the liver was reperfused for 2 hours in the I/R group; a show procedure was done in the C group. Blood samples were obtained after exposure of the hepatic hilum (T1) and 2 hours after reperfusion in the I/R group (T2) and 2.5 hours after T1 in the C group (T2). We measured glucose and insulin plasma concentrations. We determined the expressions of insulin signaling proteins, including insulin receptor (IR) β unit (IR β), IR substrate 1 (IRS-1), IRS-2, and P85 in phosphatidylinositol 3-kinase (PI3K) and tyrosine phosphorylation of these proteins in liver and skeletal muscle.

Results: Plasma glucose concentrations increased in both groups at T2 (P < .01) and were higher in the I/R group (P < .01). Insulin concentrations in the I/R group did not change significantly at T2. Insulin concentrations at T2 were higher than those at T1 in the C group (P < .05). Expressions of insulin signal proteins showed no significant difference between the 2 groups; however, tyrosine phosphorylation of IR β, IRS-1, IRS-2, and the interactions between IRS-1 in skeletal muscle or IRS-2 in liver and PI3K were significantly lower in the I/R group than the C group.

Conclusion: Hepatic I/R inhibited insulin secretion and induced insulin resistance via down-regulation during the early steps in insulin signaling in rats.

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