Glucose utilization in Type 1 (insulin-dependent) diabetes: Evidence for a defect not reversible by acute elevations of insulin

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Abstract
It has long been assumed that replacement of insulin in insulin-deficient diabetic patients will normalise glucose utilization. In this study, glucose utilization was measured in nine long-standing, poorly controlled diabetic patients and five control subjects, matched for age (33±3 versus 33±2 years) and ponderal index (22.9±1.3 versus 21.7±1.0). Glucose uptake was measured during steady state insulinaemia in the diabetic patients and control subjects, at euglycaemia (5.5±0.5 versus 5.4±0.3 mmol/l, respectively) and moderate hyperglycaemia (11.8±0.9 versus 10.2±0.7 mmol/l, respectively). At euglycaemia with similar free insulin levels (50±19 versus 43±9 mU/l; p> 0.6), the diabetic patients utilized less glucose than the control subjects (27.8±4.2 versus 56.4±5.7 μmol · kg-1.min-1; · p< 0.005). During hyperglycaemia, the diabetic patients utilized almost as much glucose as the control subjects did at euglycaemia (49.9±6.4 versus 56.4±5.7 μmol·kg-1 · min-1, respectively). In the control subjects, a 1-mmol/l rise in glucose concentration (with insulin remaining constant) resulted in a 12.3±1.3 μmol·kg-1·min-1 rise in glucose utilization. In contrast, in the diabetic patients, a 1-mmol/l rise in blood glucose resulted in a rise in glucose utilization of only 3.8±0.8 μmol · kg-1 · min-1 (p< 0.001), in the presence of similar concentrations of plasma insulin. This defect of glucose utilization in Type1 diabetic patients could not be reversed by acutely raising insulin to 247±23 mU/l. It is concluded that poorly controlled, insulin-dependent diabetes has a marked defect in glucose utilization that cannot be corrected by short-term hyperinsulinaemia.