Patients with Type 2 diabetes who are carriers for the A allele of the uncoupling protein 2 gene (UCP2) variant G-866A have lower survival rates post-myocardial infarction (MI) than non-diabetic carriers, report researchers.

The UCP2 G-866A variant is found in the promoter region of the gene and influences the level of expression of the UCP2 protein. It has also been associated with increased levels of oxidative stress markers and future risk of coronary heart disease-related events in individuals with and without Type 2 diabetes.

In this study, Barry Palmer (University of Otago, Christchurch, New Zealand) and team assessed the effect of the G-866A variant on 5-year survival in a cohort of 793 nondiabetic and 108 diabetic post-MI patients.

The overall genotype frequencies for UCP2 G-866A were 15.5%, 45.5%, and 39.0% for AA, GA, and GG genotype individuals, respectively.

G-866A genotype was not associated with survival in the overall cohort, with a 5-year mortality of 15.6%, 16.8%, and 19.4% for AA, GA, and GG genotype individuals, respectively.

But diabetic patients who were A allele carriers (AA+GA) had a higher mortality than GG homozygotes. The attributable risk for death for AA and GA genotype diabetics was 23.3% and 18.7%, respectively.

Levels of the proinflammatory enzyme myeloperoxidase were also higher in diabetic A allele carriers compared with GG homozygotes, although this association was only significant in male patients with Type 2 diabetes (64.3 vs 44.9 ng/ml).

“A growing body of evidence supports the UCP2 G-866A polymorphism as a marker of cardiovascular risk,” say Palmer et al.

They conclude in the journal Cardiovascular Diabetology: “Our data provide support for the idea that modulation of UCP2 expression might be an important novel target for reducing cardiovascular morbidity and mortality, particularly amongst diabetic patients.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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