Purple sweet potato color attenuates hepatic insulin resistance via blocking oxidative stress and endoplasmic reticulum stress in high-fat-diet-treated mice.

Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, has been reported to possess a variety of health-promoting properties. Emerging evidence indicates that PSPC can suppress postprandial hyperglycemia via inhibition of α-glucosidases. However, the protective effects of PSPC on hepatic insulin resistance and the precise mechanisms underlying these protective effects have never been investigated. In this study, our data showed that PSPC effectively improved the fasting blood glucose level, glucose and insulin tolerance by suppressing reactive oxygen species (ROS) production and by restoring glutathione (GSH) content and antioxidant enzymes' activities. PSPC further prevented the oxidative-stress-mediated endoplasmic reticulum (ER) stress in the livers of high-fat-diet (HFD)-treated mice. Moreover, PSPC dramatically suppressed the c-Jun-N-terminal kinase 1 and I kappa B kinase β activation and nuclear factor-kappa B p65 nuclear translocation caused by oxidative and ER stress in the livers of HFD-treated mice. Ultimately, PSPC notably restored the impairment of the insulin receptor substrate-1/phosphoinositide 3 kinase/protein kinase B (Akt) insulin signaling in the livers of HFD-treated mice. In conclusion, our findings indicate that PSPC protected against HFD-induced hepatic insulin resistance via decreasing ROS level and blocking ROS-mediated ER stress.