A study of obese hyperinsulinemic rats that exhibit defective dopamine receptor function in the proximal tubules shows that rosiglitazone reverses this defect, researchers at the University of Houston report. The finding suggests that insulin has a direct role in regulating dopamine D1 receptors.
The investigators previously found that in obese Zucker rats, dopamine is unable to inhibit sodium-potassium-ATPase (NaK-ATPase) and sodium-hydrogen-exchange in the kidneys because of D1 receptor dysfunction. In the December issue of Hypertension, a publication of the American Heart Association, they report on experiments in which such rats were treated with rosiglitazone, 10 mg/kg daily for 4 weeks. A group of untreated lean and obese Zucker rats served as controls.
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