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Diabetes Res Clin Pract. 1992 Mar;15(3):213-8.

Sepsis inhibits insulin-stimulated glucose transport in isolated rat adipocytes.

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Third Department of Internal Medicine, Yamagata University School of Medicine, Japan.


To assess the mechanism of insulin resistance in sepsis, we investigated insulin receptor binding and glucose uptake in isolated rat epididymal adipocytes. Male Sprague-Dawley (SD) rats weighing 200-220 g were submitted to cecal ligation under chloral hydrate anesthesia, followed by double punctures with 18-G needle into the ligated portion to produce peritonitis. Age-matched SD rats without operation were used as the controls. After starvation for 16 h, blood samples were taken from the inferior vena cava for bacterial culture and assayed for plasma glucose and IRI levels, and then adipocytes were isolated from the dissected epididymal fat tissues. Plasma levels of both glucose and IRI in septic rats were higher than those in the controls. The [125I]-insulin binding rate of the adipocytes in septic rats was similar to that of the controls. However, [3H]-2-deoxy-D-glucose uptake by adipocytes was markedly decreased in the septic group (approximately 45% of the control group at the plateau). In conclusion, this study suggests that insulin resistance in the septic state results, at least partly, from impairment in the post-binding level of the insulin receptor.

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