INTRAVENOUS INSULIN SIMULATES EARLY INSULIN PEAK AND REDUCES POSTPRANDIAL HYPERGLYCEMIA HYPERINSULINEMIA IN TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS

In NIDDM patients the deficient initial rise in insulin is a consistent finding. This early phase of insulin secretion influences the degree of hyperglycaemia following a meal. In this study insulin was infused intravenously into newly diagnosed NIDDM patients in an attempt to mimic the non-diabetic insulin response to a mixed meal and to determine the effect of early insulin availability on post-prandial glucose, C-peptide and insulin concentrations in NIDDM patients. The study involved standardized meal tolerance tests (MTT) with and without insulin on 2 separate days, 1 week apart. Insulin was given by intravenous infusion (2.5 U Actrapid over 30 min) immediately following the start of a 500 kcal MTT. The subjects were divided into non-obese and obese sub-groups with 8 subjects in each group (BMI 24.0 vs 32.0 kg/m2, HbA1 12.7 vs 9.8%, age 44.4 vs 43.0 yrs, respectively). Following intravenous insulin in non-obese diabetics a peak plasma insulin concentration of 0.393 pmol/ml was observed at 15 min compared to 0.148 pmol/ml at 90 min without exogenous insulin. The post-prandial glucose excursion between 60 and 120 min was significantly lowered with insulin (p < 0.01). Similarly in the obese patients a higher and earlier insulin peak was achieved with intravenous insulin, with a lower level during the second half of the 4 h post-prandial period, the difference reaching significance at 150 min (p < 0.05). No differences were observed in the C-peptide concentrations between the 2 study days. In 5 obese patients given 2 serial test meals on the same day an earlier insulin peak was consistently followed by reduced post-prandial hyperinsulinaemia in response to the low dose prandial insulin infusions. This study demonstrates that an early peak of insulin reduces post-prandial hyperglycaemia in both non-obese and obese NIDDM, and also has the additional benefit of reducing post-prandial hyperinsulinaemia particularly in obese NIDDM patients.