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Mechanisms of Hemorrhage-Induced Hepatic Insulin Resistance: Role of Tumor Necrosis Factor-{alpha}
Ma et al.
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Hemorrhage induces the rapid development of hepatic insulin resistance
Ma et al.
Am. J. Physiol. Gastrointest. Liver Physiol. 2003;284:G107-G115.
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The Relationship of Insulin Production to Glucose Metabolism in Severe Sepsis
Dahn et al.
Arch Surg 1985;120:166-172.
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Alterations in Cell Function With Ischemia and Shock and Their Correction
Chaudry et al.
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Studies of Peripheral Glucose Uptake During Sepsis
Wichterman et al.
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Cuthbertson and Zagreb
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hours. Basal glucose uptake by isolated soleus muscle from ADX normal rats and ADX rats subjected to shock ("shock" muscles) increased with the increase in medium glucose concentration and uptake was similar in both groups of muscles. This indicates that shock per se did not produce any alterations in the basal glucose carrier mechanism. Insulin (0.1 unit/ml) increased uptake in ADX control but not in ADX shock muscles. Maximal stimulation of glucose uptake in shock muscles was observed at an insulin concentration of 0.2 unit/ml insulin. These experiments provide the first direct evidence that the responsiveness of tissues to insulin is altered during shock. This alteration could not be due to increased steroid or epinephrine output during shock.