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Curr Med Res Opin. 2005 Jul;21(7):989-98.

Contributions of basal and post-prandial hyperglycaemia to micro- and macrovascular complications in people with type 2 diabetes.

Author information

1
University of Newcastle upon Tyne, Newcastle upon Tyne, UK. philip.home@newcastle.ac.uk

Abstract

BACKGROUND:

People with Type 2 diabetes mellitus are at high risk of cardiovascular disease and microvascular complications. A number of epidemiological studies have shown a strong relationship between the prevalence of vascular complications and raised levels of plasma glucose and glycated haemoglobin (HbA(1c)). Accumulating evidence supports the superior independent prognostic importance of the post-challenge glucose level, measured either 1 or 2 h after a glucose load. Thus, data from studies conducted in Europe, the USA, and particularly the Pacific rim and South Asia suggest that 2-h glucose is a better predictor of cardiovascular and all-cause mortality than pre-breakfast glucose, both in people with diabetes and those with pre-diabetic impaired glucose tolerance (IGT). Pathophysiological studies suggest that post-prandial rises in hyperglycaemia can trigger endothelial damage through multiple mechanisms, including increased oxidative stress and the increased expression of atherogenic circulating adhesion molecules and inflammatory cytokines that induce and regulate cell recruitment, migration, growth, and proliferation. Optimal pharmacological control of meal-time glucose levels can help to lower the HbA(1c) and thus may reduce the incidence of vascular complications in many people with diabetes. Moreover, emerging evidence suggests that reducing meal-time hyperglycaemia may delay the progression from pre-diabetic states toward overt diabetes.

SCOPE:

This review (based on MEDLINE searches, 1980-2005) examines the evidence linking the microvascular and macrovascular complications of diabetes and glycaemic control, assesses the relative contributions of basal and meal-time concentrations, and considers the implications for optimal treatment for people with Type 2 diabetes or with prediabetic IGT.

PMID:
16004665
DOI:
10.1185/030079905x49662
[Indexed for MEDLINE]

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