The role of stimulating NO bioavailability by statins in treating insulin resistance is addressed in a study from Switzerland. The authors of " Simvastatin Prevents High-Fat Diet-Diet-Induced Arterial Hypertension and Metabolic Insulin Resistance in Partially eNOS Deficient Mice," are Stphane Cook, MD, Peter Vollenweider, MD and Urs Scherrer, MD, all at the Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. Their findings are being presented at the American Physiology Society sponsored conference, Experimental Biology 2003, being held April 11-15, 2003, at the San Diego Conference Center, San Diego, CA.
Simvastatin or vehicle treated eNOS+/- and eNOS-/- mice were fed a high-fat diet or normal chow for eight weeks. Arterial pressure and insulin sensitivity (glucose infusion rate during euglycemic hyperinsulinemic clamp) were measured at the end of this eight week period.
High-fat diet caused arterial hypertension and insulin resistance in eNOS+/- mice. Simvastatin prevented both the high-fat diet-induced insulin resistance and arterial hypertension in eNOS+/- mice. In contrast, simvastatin did not attenuate high-fat diet induced arterial hypertension and insulin resistance in eNOS-/- mice.
These findings provide the first evidence that simvastatin prevents diet-induced arterial hypertension and insulin resistance in mice. This effect appears to be related to stimulation of vascular NO availability (as evidenced by the results in eNOS-/- mice). These data suggest that simvastatin may help to combat the epidemic of insulin resistance and hypertension in humans.