Postprandial hyperglycaemia in type 2 diabetes: pathophysiological aspects, teleological notions and flags for clinical practice

Abstract

Type 2 diabetes subjects carry an excess risk for micro- and macrovascular disease and a higher cardiovascular morbidity and mortality rate. The beneficial impact of tight glycaemic control - evidenced by the integrated marker of fasting glucose and postprandial glucose values, the HbA(1c) - for the prevention of microvascular complications is definitely confirmed. Over the past few years, several studies have identified postprandial hyperglycaemia as a better predictor of cardiovascular or even of all-cause mortality, as well as an independent risk factor for atherosclerosis. The continuous glucose monitoring could offer a rationale means for the detection of postprandial hyperglycaemia and ultimately for its effective management. Advances in technology keep a promise for a reliable, convenient and closer to the idea of the artificial endocrine pancreas glucose sensor. Subcutaneous glucose levels charted by one of the new sensors were found to be well correlated with venous glucose measurements. Intervention for a healthy lifestyle is frequently hampered by patients’ poor compliance. The availability of diverse antidiabetic agents provides options for targeting the glycaemic goal and a choice more fitted to the particularized pathophysiology of each individual subject. Drugs targeting postprandial glycaemia may prove to represent the ‘sine qua non’ for the ‘return’ of postprandial glucose values at a ‘non-deleterious’ threshold, either as monotherapy for the early stages of the disease or as combination therapy later in the progression of diabetes. Copyright (C) 2004 John Wiley Sons, Ltd

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