College of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, China.
Department of pharmacy, The first Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, China.
Diab Vasc Dis Res. 2020 Nov-Dec;17(6):1479164120966998. doi: 10.1177/1479164120966998.
The objective of this study was to explore the effects of epigallocatechin-3-gallate (EGCG) on type 2 diabetes mellitus (T2DM).
Male Sprague-Dawley rats were allocated into six groups. The control group received a conventional diet. The diabetic group received a high-sucrose high-fat (HSHF) diet for 4 weeks and then was fasted and injected with streptozotocin (STZ); subsequently, the rats received a HSHF diet for another 4 weeks to develop diabetes. The four treatment groups were diabetic rats that received intragastric metformin (500 mg/kg/day) or EGCG (25, 50, and 100 mg/kg/day) for 10 weeks. All groups except the control group received a HSHF diet throughout the experiment. Several biochemical parameters such as fasting blood glucose (FBG), postprandial blood glucose (PBG), liver glycogen, muscle glycogen, fasting serum insulin (FSI), homeostasis model of insulin resistance (HOMA-IR), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), free fatty acids (FFA), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured to assess the effects of EGCG on glycemic control, insulin resistance, lipid profile, and oxidative stress. Furthermore, oxidative stress in pancreatic islet β cells was detected by dihydroethidium staining.
A HSHF diet and STZ injection induced T2DM, as indicated by changed blood glucose and body weight, which was accompanied by insulin resistance, an altered lipid profile, and oxidative stress. Interestingly, EGCG treatment dose-dependently recovered these indexes.
EGCG successfully ameliorated glycemic control and insulin sensitivity while reducing the lipid profile and oxidative stress in a T2DM rat model.
本研究旨在探讨表没食子儿茶素没食子酸酯（EGCG）对 2 型糖尿病（T2DM）的影响。
雄性 Sprague-Dawley 大鼠分为 6 组。对照组给予常规饮食。糖尿病组给予高蔗糖高脂肪（HSHF）饮食 4 周，然后禁食并注射链脲佐菌素（STZ）；随后，大鼠继续给予 HSHF 饮食 4 周以诱发糖尿病。4 个治疗组为糖尿病大鼠，分别给予盐酸二甲双胍（500mg/kg/天）或 EGCG（25、50 和 100mg/kg/天）灌胃 10 周。除对照组外，所有组在整个实验过程中均给予 HSHF 饮食。测量空腹血糖（FBG）、餐后血糖（PBG）、肝糖原、肌糖原、空腹血清胰岛素（FSI）、胰岛素抵抗稳态模型评估（HOMA-IR）、总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、游离脂肪酸（FFA）、超氧化物歧化酶（SOD）和丙二醛（MDA）等生化参数，以评估 EGCG 对血糖控制、胰岛素抵抗、血脂谱和氧化应激的影响。此外，通过二氢乙啶染色检测胰岛β细胞的氧化应激。
HSHF 饮食和 STZ 注射诱导了 T2DM，表现为血糖和体重的变化，同时伴有胰岛素抵抗、血脂谱改变和氧化应激。有趣的是，EGCG 治疗呈剂量依赖性地恢复了这些指标。
EGCG 成功改善了 T2DM 大鼠模型的血糖控制和胰岛素敏感性，同时降低了血脂谱和氧化应激。
