The ergogenic supplement β-hydroxy-β-methylbutyrate (HMB) attenuates insulin resistance through suppressing GLUT-2 in rat liver
The ergogenic supplement β-hydroxy-β-methylbutyrate (HMB) attenuates insulin resistance through suppressing GLUT-2 in rat liver
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DOI：
10.1139/cjpp-2015-0385
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发表时间：
2016-05-01
影响因子：
2.1
通讯作者：
Gameil, Nariman M.
中科院分区：
文献类型：
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作者：
Sharawy, Maha H.;El-Awady, Mohammed S.;Gameil, Nariman M.
本研究探讨了β -羟基- β -甲基丁酸酯（HMB）对高果糖饮食（HFD）大鼠胰岛素抵抗的影响。雄性Sprague Dawley大鼠分别饲喂60% HFD和320 mg.kg(-1) HMB喂养12周。第1天(1)，口服)，连续4周。HFD显著提高了空腹胰岛素、空腹血糖、糖化血红蛋白（HBA1C）、肝糖原含量和胰岛素抵抗（HOMA-IR）指数，同时降低了葡萄糖和胰岛素耐受。此外，HFD显著提高了血清甘油三酯（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）水平，同时显著降低了高密度脂蛋白胆固醇（HDL-C）。此外，HFD显著增加了肝脏中葡萄糖转运蛋白2型（GLUT-2）、哺乳动物雷帕霉素靶蛋白（mTOR）和甾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α (ppar - α)的mRNA表达。主动脉对乙酰胆碱（ACh）的舒张功能受损，组织病理学显示严重的肝脂肪变性。HMB显著增加胰岛素耐量，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ach诱导的松弛，改善肝脂肪变性，降低GLUT-2 mRNA表达。综上所述，HMB可能通过抑制肝脏GLUT-2来减轻胰岛素抵抗和肝脏脂肪变性。
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.