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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The ergogenic supplement beta-hydroxy-beta-methylbutyrate (HMB) attenuates insulin resistance through suppressing GLUT-2 in rat liver
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The ergogenic supplement beta-hydroxy-beta-methylbutyrate (HMB) attenuates insulin resistance through suppressing GLUT-2 in rat liver

机译：人体工学补充剂β-羟基-β-甲基丁酸（HMB）通过抑制大鼠肝脏中的GLUT-2减轻胰岛素抵抗

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摘要

This study investigates the effect of the ergogenic supplement beta-hydroxy-beta-methylbutyrate (HMB) on insulin resistance induced by high-fructose diet (HFD) in rats. Male Sprague Dawley rats were fed 60% HFD for 12 weeks and HMB (320 mg.kg(-1).day(-1), orally) for 4 weeks. HFD significantly increased fasting insulin, fasting glucose, glycosylated hemoglobin (HBA1C), liver glycogen content, and homeostasis model assessment of insulin resistance (HOMA-IR) index, while it decreased glucose and insulin tolerance. Furthermore, HFD significantly increased serum triglycerides (TG), low density lipoprotein cholesterol (LDL-C), and very low density lipoprotein cholesterol (VLDL-C) levels, while it significantly decreased high density lipoprotein cholesterol (HDL-C). Moreover, HFD significantly increased mRNA expression of glucose transporter type-2 (GLUT-2), the mammalian target of rapamycin (mTOR), and sterol regulatory element-binding protein-1c (SREBP-1c) but decreased peroxisome proliferator-activated receptor-alpha (PPAR-alpha) in liver. Aortic relaxation to acetylcholine (ACh) was impaired and histopathology showed severe hepatic steatosis. HMB significantly increased insulin tolerance and decreased fasting insulin, HOMA-IR, HBA1C, hepatic glycogen content, serum TG, LDL-C, and VLDL-C. Additionally, HMB enhanced ACh-induced relaxation, ameliorated hepatic steatosis, and decreased mRNA expression of GLUT-2. In conclusion, HMB may attenuate insulin resistance and hepatic steatosis through inhibiting GLUT-2 in liver.
机译：这项研究调查了高剂量果糖饮食（HFD）对大鼠产生的人源性补充β-羟基-β-甲基丁酸（HMB）的胰岛素抵抗的作用。将60％HFD的雄性Sprague Dawley大鼠喂食12周，口服HMB（320 mg.kg（-1）.day（-1））喂食4周。 HFD显着增加了空腹胰岛素，空腹葡萄糖，糖基化血红蛋白（HBA1C），肝糖原含量和胰岛素抵抗（HOMA-IR）指数的稳态模型评估，同时降低了葡萄糖和胰岛素耐受性。此外，HFD显着提高了血清甘油三酸酯（TG），低密度脂蛋白胆固醇（LDL-C）和极低密度脂蛋白胆固醇（VLDL-C）的水平，同时却显着降低了高密度脂蛋白胆固醇（HDL-C）。此外，HFD显着提高了2型葡萄糖转运蛋白（GLUT-2），哺乳动物雷帕霉素靶标（mTOR）和固醇调节元件结合蛋白1c（SREBP-1c）的mRNA表达，但降低了过氧化物酶体增殖物激活受体-肝中的α（PPAR-α）。主动脉对乙酰胆碱（ACh）的松弛受到损害，组织病理学显示严重的肝脂肪变性。 HMB可显着提高胰岛素耐受性，并降低空腹胰岛素，HOMA-IR，HBA1C，肝糖原含量，血清TG，LDL-C和VLDL-C。此外，HMB增强了ACh诱导的松弛，改善了肝脂肪变性，并降低了GLUT-2的mRNA表达。总之，HMB可通过抑制肝脏中的GLUT-2减轻胰岛素抵抗和肝脂肪变性。

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