Mechanism of hyperinsulinemia in endotoxicosis

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Abstract
Hyperinsulinemia subsequent to endotoxemia is a key factor leading to the disturbance of glucose homeostasis in endotoxin shock. This study investigated the mechanism(s) of hyperinsulinemia during endotoxicosis (Salmonella-enteritidis) in the rat. Two primary mechanisms for the hyperinsulinemia were evaluated: decreased removal of insulin by the endotoxic liver; increased of insulin by the endotoxic pancreas. Endotoxin treatment of donor rats did not impair the removal of TCA[tri chloroacetic acid]-precipitable 125I-labeled insulin by the isolated perfused liver. Perfused pancreases from endotoxic donors secreted more insulin than control pancreases in response to a provocative stimulus of glucose. In vivo measurements of plasma immunoreactive insulin and glucose indicated an elevated hepatic portal vein insulin:glucose ratio associated with endotoxicosis. The hyperinsulinemia of endotoxicosis is due primarily to hypersecretion of insulin by the endotoxic pancreas.