a Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province 221116, PR China.
b Key Laboratory of Biology and Genetic Improvement of Sweetpotato, Ministry of Agriculture, Jiangsu Xuzhou Sweetpotato Research Center, Xuzhou 221131, Jiangsu Province, PR China.
Appl Physiol Nutr Metab. 2017 Oct;42(10):1082-1091. doi: 10.1139/apnm-2016-0635. Epub 2017 Jun 21.
Our previous work showed that purple sweet potato colour (PSPC), a class of naturally occurring anthocyanins, effectively improved hepatic glucose metabolic dysfunction in high-fat-diet (HFD)-treated mice. This study investigated the effects of PSPC on HFD-induced hepatic steatosis and the signalling events associated with these effects. Mice were divided into 4 groups: control group, HFD group, HFD+PSPC group, and PSPC group. PSPC was administered daily for 20 weeks at oral doses of 700 mg/(kg·day)). Our results showed that PSPC significantly improved obesity and related metabolic parameters, as well as liver injury in HFD-treated mice. Moreover, PSPC dramatically attenuated hepatic steatosis in HFD-treated mice. PSPC markedly prevented oxidative stress-mediated Src activation in HFD-treated mouse livers. Furthermore, PSPC feeding remarkably suppressed mitogen-activated protein kinase kinase/extracellular-signal-regulated kinase (MEK/ERK) signalling and consequent CCAAT/enhancer binding protein β (C/EBPβ) activation and restored AMPK activation in HFD-treated mouse livers, which was confirmed by U0126 treatment. Ultimately, PSPC feeding dramatically reduced protein expression of FAS and CD36 and the activation of ACC, and increased the protein expression of CPT1A in the livers of HFD-treated mice, indicating decreased lipogenesis and fatty acid uptake and enhanced fatty acid oxidation. In conclusion, PSPC exhibited beneficial effects on hepatic steatosis, which were associated with blocking Src and C/EBPβ activation.
我们之前的工作表明，紫薯花色苷（PSPC），一类天然存在的花青苷，可有效改善高脂肪饮食（HFD）处理的小鼠的肝葡萄糖代谢功能障碍。本研究旨在探讨 PSPC 对 HFD 诱导的肝脂肪变性的影响及其作用的相关信号事件。将小鼠分为 4 组：对照组、HFD 组、HFD+PSPC 组和 PSPC 组。PSPC 以 700mg/（kg·天）的剂量经口给药 20 周。我们的结果表明，PSPC 可显著改善肥胖及相关代谢参数，并减轻 HFD 处理的小鼠的肝损伤。此外，PSPC 可显著减轻 HFD 处理的小鼠的肝脂肪变性。PSPC 可显著预防氧化应激介导的 Src 激活。此外，PSPC 喂养可显著抑制 HFD 处理的小鼠肝脏中丝裂原活化蛋白激酶激酶/细胞外信号调节激酶（MEK/ERK）信号通路及随后的 CCAAT 增强子结合蛋白 β（C/EBPβ）的激活，并恢复 AMPK 的激活，这一结果得到 U0126 处理的验证。最终，PSPC 喂养可显著降低 FAS 和 CD36 的蛋白表达及 ACC 的激活，并增加 HFD 处理的小鼠肝脏中 CPT1A 的蛋白表达，表明脂肪生成和脂肪酸摄取减少，脂肪酸氧化增强。总之，PSPC 对肝脂肪变性具有有益作用，其机制与阻断 Src 和 C/EBPβ 的激活有关。
