Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway
Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway
复制标题
不同储藏年份客家炒茶激活AMPK/ACC/CPT1通路对高脂饮食诱导肥胖小鼠模型的抗肥胖和抗炎作用
DOI：
10.29219/fnr.v64.1681
复制
发表时间：
2020-06-08
影响因子：
3.3
通讯作者：
Sun, Shili
中科院分区：
文献类型：
--
作者：
Li, Qiuhua;Lai, Xingfei;Sun, Shili
研究背景肥胖是代谢综合征的典型代表，也是心血管疾病的高危因素之一。因此，预防和治疗肥胖已逐渐成为一项全球性运动。绿色茶对预防肥胖有效的报道很多，但作为一种具有地域特色的绿色茶，目前还没有不同存放年限的客家炒茶（HT）有减肥效果的报道。目的探讨HT对饮食诱导的肥胖小鼠的影响。方法将小鼠随机分为5组：正常对照组、肥胖模型组、HT 2003、HT 2008、HT 2015组，分别给予正常对照组、高脂饲料组、不同贮存年限的HT治疗6周。结果HT可降低血清和肝脏甘油三酯水平;降低肝脏/体重比;降低附睾、肾周和肠系膜脂肪堆积;降低肝脏脂肪变性程度;降低脂肪细胞肥大，并伴有体重减轻。此外，HT还能降低肥胖小鼠肝组织中促炎细胞因子肿瘤坏死因子α（TNF α）、诱导型一氧化氮合酶（iNOS）、环氧合酶-2（考克斯-2）的表达水平，降低脂肪酸合酶（FAS）活性。此外，HT处理还增加了参与FAS途径的AMP活化蛋白激酶（AMPK）及其直接下游蛋白乙酰辅酶A羧化酶（ACC）和肉毒碱棕榈酰转移酶I（CPT-1）的磷酸化。结论HT通过激活AMPK/ACC/CPT 1通路对高脂饮食诱导的肥胖小鼠具有潜在的保护作用，且在一定程度上与3种HT的储存时间无关。
Background As a typical representative of metabolic syndrome, obesity is also one of the extremely dangerous factors of cardiovascular diseases. Thus, the prevention and treatment of obesity has gradually become a global campaign. There have been many reports that green tea is effective in preventing obesity, but as a kind of green tea with regional characteristics, there have been no reports that Hakka stir-fried tea (HT) of different storage years has a weight loss effect. Aims The aim was to investigate the effect of HT in diet-induced obese mice. Methods The mice were divided into five groups as follows: the control group received normal diet; the obese model group received high-fat diet; and HT2003, HT2008, and HT2015 groups, after the induction of obesity via a high-fat diet, received HT of different storage years treatment for 6 weeks, respectively. Results It was observed that HT decreased the levels of serum and liver triglyceride; the ratio of liver to body weight; accumulation of epididymal, perirenal, and mesenteric fat; the degree of hepatic steatosis; and adipocyte hypertrophy, with the concomitant reduction of body weight. Moreover, HT decreased the expression levels of proinflammatory cytokines tumor necrosis factor α (TNF α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and reduced fatty acid synthase (FAS) activity in liver tissue of obese mice. In addition, HT treatment also increased the phosphorylation of AMP-activated protein kinase (AMPK) and its direct downstream proteins, acetyl coenzyme A carboxylase (ACC), and carnitine palmitoyltransferase I (CPT-1), which participate in FAS pathway. Conclusions These findings demonstrate that HT treatment has a potential protection on high-fat diet-induced obesity mice via activating the AMPK/ACC/CPT1 pathway, and to a certain extent, it has nothing to do with the storage time of three kinds of HT.