(HealthDay)—Treating mice fed a high-fat diet with telmisartan reverses insulin resistance and glucose intolerance, but only when the peroxisome proliferator-activated receptor-δ (PPAR-δ) gene is present, according to a study published online Dec. 13 in Diabetes.
Li Li, from the Chongqing Institute of Hypertension in China, and colleagues examined the effects of telmisartan, an angiotensin receptor blocker, on insulin signaling and glucose uptake in wild-type mice and mice lacking the PPAR-δ gene in muscle.
The researchers found that, in cultured myotubes, treatment with telmisartan correlated with increased PPAR-δ expression and activated transcriptional activity of PPPAR-δ. In cultured myotubes with palmitate-induced insulin-resistance, enhanced insulin-stimulated phosphorylation of Akt and Akt substrate of 160 kDa as well as translocation of Glu4 to the plasma membrane was seen with telmisartan treatment. Antagonizing PPAR-δ or phosphatidylinositol-3 kinase inhibited these effects. In cultured myotubes, insulin-stimulated glucose uptake which was reduced by palmitate could be restored by telmisartan. Similar results were observed in vivo in wild-type mice, but not PPAR-δ knockout mice, with telmisartan reversing high-fat diet-induced insulin resistance and glucose intolerance.
"In summary, we demonstrate that telmisartan has a profound role in the improvement of glucose homeostasis in skeletal muscle, which is associated with activation of the PPAR-δ/phosphatidylinositol 3-kinase pathway," Li and colleagues conclude. "These findings implicate PPAR-δ as a potential therapeutic target in the treatment of hypertensive subjects with insulin resistance."
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