Department of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju, Korea.
Department of Food and Nutrition, Kyung Hee University, Seoul, Korea.
Metabolism. 2014 May;63(5):693-701. doi: 10.1016/j.metabol.2014.02.003. Epub 2014 Feb 11.
Resveratrol (RSV) regulates NAD bioavailability and sirtuin-related metabolism, which relates to aging, metabolic syndrome and non-alcoholic fatty liver disease. The purpose of this study was to investigate the effects of resveratrol on hepatic metaflammation in a rodent model of high-fat (HF) diet-induced obesity (DIO).
MATERIALS/METHODS: DIO was induced in a subset of mice given an HF diet (45% kcal fat). After 6weeks of HF diet feeding, RSV was delivered via an osmotic pump for 4weeks. The experimental groups were as follows: 1) lean control fed with a standard diet, 2) HF diet-induced obese control, and 3) HF_RSV (8mg/kg/day). After 4weeks of each treatment, blood and liver tissues were collected and the indices of glucose control, serum and liver triglyceride (TG), sirtuin pathway, inflammation, and NOD-like receptor family, pryin domain containing 3 (NLRP3) inflammasome were analyzed.
Body weight and food intake were not altered by administering resveratrol. Glucose control was impaired, and serum and liver TG levels were increased by the HF diet. Hepatic inflammation was aggravated in mice fed with the HF diet, as shown by the increased levels of the pro-inflammatory markers interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha in the liver. However, resveratrol administration significantly improved glucose control, and serum and liver TG contents. Also, resveratrol treatment reduced the levels of the pro-inflammatory markers. These improvements were accompanied by alterations in sirtuin pathway and NLRP3 inflammasome activation.
These results demonstrate that resveratrol ameliorates hepatic metaflammation, accompanied by alterations in NLRP3 inflammasome.
白藜芦醇（RSV）调节 NAD 生物利用度和与衰老、代谢综合征和非酒精性脂肪性肝病相关的代谢途径。本研究旨在探讨白藜芦醇对高脂肪（HF）饮食诱导肥胖（DIO）啮齿动物模型肝代谢炎症的影响。
材料/方法：HF 饮食（45%卡路里脂肪）喂养一部分小鼠以诱导 DIO。HF 饮食喂养 6 周后，通过渗透泵给予 RSV 治疗 4 周。实验组如下：1）标准饮食喂养的瘦对照组，2）HF 饮食诱导的肥胖对照组，和 3）HF_RSV（8mg/kg/天）。每种治疗 4 周后，收集血液和肝脏组织，分析葡萄糖控制、血清和肝脏甘油三酯（TG）、沉默调节蛋白通路、炎症和 NOD 样受体家族，富含亮氨酸重复域蛋白 3（NLRP3）炎性体的指标。
给予白藜芦醇并未改变体重和食物摄入量。HF 饮食导致葡萄糖控制受损，血清和肝脏 TG 水平升高。HF 饮食喂养的小鼠肝脏炎症加重，肝脏中促炎标志物白细胞介素 1（IL-1）、IL-6 和肿瘤坏死因子-α水平升高。然而，白藜芦醇给药显著改善了葡萄糖控制和血清及肝脏 TG 含量。此外，白藜芦醇治疗降低了促炎标志物的水平。这些改善伴随着沉默调节蛋白通路和 NLRP3 炎性体激活的改变。
这些结果表明，白藜芦醇改善了肝代谢炎症，伴随着 NLRP3 炎性体的改变。
