Summary
Increasing evidence suggests that tight metabolic control slows or prevents the development
of diabetic complications. Various degrees of peripheral insulin resistance and inadequate
glucose-induced insulin secretory profiles are seen in Type 2 diabetes. The main deficit
in insulin release occurs early in the development of the disease and can be measured
in association with meals, when the increase in meal-related insulin secretion is
delayed and sluggish (first-peak/early-phase defect). The consequences of this are
high postprandial blood glucose concentrations and overall loss of glycaemic control.
Improved prandial glucose metabolism will lead to an overall improvement in glycaemic
control. The new concept of prandial glucose regulation, aimed at improving or restoring
meal-related insulin secretion, has led to the development of repaglinide, a carbamoyl-methyl
benzoic acid derivative, in the treatment of Type 2 diabetes. Patients treated with
repaglinide using the concept 'one meal, one dose; no meal, no dose' experience improved
insulin secretion, long-term metabolic control and quality of life and reduced postprandial
hyperglycaemia. Treatment of Type 2 diabetes will be improved further through the
use of combinations of drugs with different modes of action, which will prevent or
reduce acute and chronic complications. New training programmes for physicians and
patients must be developed to optimize the available pharmacological options for treating
the extremely heterogeneous group of patients with Type 2 diabetes with a flexible
oral therapeutic concept. An interdisciplinary approach to the care of these patients
is urgently needed.
Key words
Type 2 diabetes - impaired glucose tolerance - prandial glucose regulation
