Hyperinsulinaemia and insulin insensitivity: studies in subjects with insulinoma

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Abstract
Hepatic glucose turnover, peripheral insulin sensitivity and insulin receptor binding were measured in four subjects with insulinoma before and 3 months after surgical resection of the insulinoma. Basal hepatic glucose production, quantitated employing a primed constant infusion of tritiated glucose, was low pre-operatively (5.2±1·7μmol·kg−1· min−1) but returned to normal post-operatively (14.9±2.8; normal subjects 13.9±0.8 μmol·kg−1·min−1). Paired euglycaemic dose-response curves were developed for each subject. Insulin sensitivity, expressed as a right shift of the dose-response curve (ED50), was low pre- and post-operatively. However, insulin responsiveness (Vmax) remained normal (pre-operatively 13.9±2.2, post-operatively 13.8±0.8, normal subjects 16.7±0.8ml·kg−1·min−1). There was no consistent pattern in monocyte or erythrocyte receptor binding before or after surgery. These data suggest that the chronic hyperinsulinaemia causes suppression of hepatic glucose production, and a state of insulin insensitivity which appears to be due to a post-receptor defect.