Simvastatin Treats Insulin Resistance
Cholesterol controlling drug Simvastatin fighst insulin
resistance
Over the past decade, evidence has accumulated indicating
that nitric oxide (NO) may play a key role in the
control of metabolic and cardiovascular homeostasis,
as evidenced by mice lacking the gene for endothelial
nitric oxide synthase (eNOS) that are insulin resistant
and hypertensive. An animal study now finds that
stimulating NO bioavailability by lipid lowering
statins may represent a new way to combat this epidemic.
Statins are a group of compounds that have been
used successfully to lower cholesterol and prevent
myocardial infarction. A less well known effect of
statins is that they augment NO bioavailability in
circulation. Abnormalities in the body's production
of NO have been implicated in high blood pressure,
atherosclerosis (narrowing of the arteries), diabetes,
impotence, and stroke.
One statin is the prescription drug Simvastatin,
used with diet changes (restriction of cholesterol
and fat intake) to reduce the amount of cholesterol
and certain fatty substances in the blood. Accumulation
of cholesterol and fats along the walls of the arteries
(a process known as atherosclerosis) decreases blood
flow and, therefore, the oxygen supply to the heart,
brain, and other parts of the body. Lowering your
blood level of cholesterol and fats may help to prevent
heart disease, angina (chest pain), strokes, and
heart attacks. Now this important drug could also
be instrumental in the battle against insulin resistance.
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 Stephane 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.
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