PPARδ Is Required for Exercise to Attenuate Endoplasmic Reticulum Stress and Endothelial Dysfunction in Diabetic Mice.

摘要: Physical activity has profound benefits on health, especially cardiometabolic wellness. Experiments in rodents with trained exercise have shown that improves vascular function and reduces inflammation by modulating the balance between nitric oxide (NO) oxidative stress. However, upstream regulator of exercise-induced is unclear. We aimed to investigate involvement peroxisome proliferator-activated receptor δ (PPARδ) functional improvement. show PPARδ a crucial mediator for exert beneficial effect endothelium diabetic mice. In db/db mice high-fat diet-induced obese mice, 4 weeks treadmill restored endothelium-dependent vasodilation aortas flow-mediated mesenteric resistance arteries, whereas genetic ablation Ppard abolished such improvements. Exercise induces AMPK activation subsequent activation, which help reduce endoplasmic reticulum (ER) stress, thus increasing NO bioavailability endothelial cells tissues. Chemical chaperones 4-phenylbutyric acid tauroursodeoxycholic decrease ER stress protect against dysfunction The results demonstrate PPARδ-mediated inhibition contributes provides potentially effective targets treating vasculopathy.