Improved insulin sensitivity after long-term treatment with AT1 blockers is not associated with PPARγ target gene regulation.

In both cell culture experiments and in vivo studies, a number of angiotensin II type 1 (AT(1)) receptor antagonists activated the peroxisome proliferator-activated receptor-γ (PPARγ). This mechanism has been discussed to be, at least in part, responsible for the improvement in glucose metabolism observed in animal studies and clinical trials. To investigate whether the PPARγ-dependent mechanism may represent a valid target for chronic therapy, spontaneously hypertensive rats (SHR) were fed either with a cafeteria diet (CD) or standard chow.