Approaches to the management of postprandial hyperglycaemia.
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 carbamoylmethyl 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.
Landgraf
R
R
Section of Endocrinology and Diabetology, University of Munich, Germany.
D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000503:physiopathology; D005502:Food; D006801:Humans; D006943:Hyperglycemia / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion
D007004:Hypoglycemic Agents; D007328:Insulin