(10-11-06) Calorie Restriction Improves Cardiovascular Risk Factors

via Reduction of Mitochondrial Reactive Oxygen Species in Type II Diabetic Rats.

Minamiyama Y, Bito Y, Takemura S, Takahashi Y, Kodai S, Mizuguchi S, Nishikawa Y, Suehiro S, Okada S.
Okayama University Graduate School of Medicine and Dentistry.
UCP2 is an important regulator of intracellular ROS production. We determined the effects of calorie restriction (CR) on the dynamic aspects of mitochondrial reactive oxygen species (ROS) production, uncoupling protein 2 (UCP2) and NO-cGMP pathway in the cardiovascular tissues of type II diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Some rats were on restricted diets (30% reduction from free intake) from age 29 to 42 weeks. Blood glucose, hemoglobin A1c, plasma levels of free fatty acid, triacylglycerol, and plasminogen activator inhibitor-1 in OLETF rats were significantly higher than those in non-diabetic control (LETO) rats at 29 weeks. Mitochondrial ROS production and UCP2 protein expression significantly increased in the heart and aorta of OLETF rats compared with that in LETO rats. A fibrogenic growth factor, transforming growth factor (TGF)-beta1 in the coronary vessels, endothelial NO synthase (eNOS), and aortic nitrotyrosine were increased in OLETF rats at 42 weeks. In contrast, an index of the NO-cGMP pathway, phosphorylated vasodilator-stimulated phosphoprotein and SOD activity in the aorta was significantly diminished. The relationship between UCP2 and ROS production in the cardiovascular function of diabetic rats being fed a CR diet is unknown. These abnormalities in OLETF rats were reversed to normal levels by CR. CR significantly improved the NO-cGMP pathway via normalizing ROS generation in OLETF rats. Decrease of UCP2 expression by CR may be a compensatory mechanism to counteract decreased intracellular oxidative stress. The data suggest that CR may prevent cardiovascular tissues from oxidative stress provoked by diabetes mellitus.

Source: J Pharmacol Exp Ther.

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