Antioxidants · 3 authors, 5 centres
This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.
Male C57Bl/6J mice fed a western-style diet high in fat and processed carbohydrates for 16 weeks showed reduced smooth muscle cell and endothelial cell death in posterior cerebral arteries during acute H2O2 exposure, whereas mice fed a high-fat diet inducing obesity did not. The protection was mediated by limiting Ca2+ influx through TRPV4 and TRPC3 channels.
Male C57Bl/6J mice were fed a western-style diet (WD), a high-fat obesity-inducing diet (DIO), or respective control diets for 16 weeks. Posterior cerebral arteries were isolated, pressurized, and exposed to H2O2 (200 µM) for 50 minutes. Smooth muscle cell and endothelial cell death were reduced in arteries from WD-fed mice but not DIO-fed mice compared to controls. WD selectively attenuated mitochondrial membrane potential depolarization and vessel wall Ca2+ influx during H2O2 exposure. Inhibition of TRPV4 or TRPC3 channels reduced cell death and Ca2+ responses in control-diet arteries and eliminated differences between control and WD groups. Src kinase inhibition reduced smooth muscle cell death and Ca2+ responses only in control-diet arteries, eliminating diet differences, but did not alter endothelial cell death. These preclinical findings suggest processed carbohydrates, rather than fat alone, drive vascular adaptations that limit oxidative stress-induced cell death.
