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给予生物素可预防 Otsuka Long-Evans Tokushima Fatty 大鼠骨骼肌胰岛素抵抗的发生。

Administration of biotin prevents the development of insulin resistance in the skeletal muscles of Otsuka Long-Evans Tokushima Fatty rats.

机构信息

Laboratory of Nutrition, Department of Science of Food Function and Health, Graduate School of Agricultural Science, Tohoku University, 1-1 Tsutsumidori-Amamiyamachi, Sendai 981-8555, Japan.

出版信息

Food Funct. 2012 Apr;3(4):414-9. doi: 10.1039/c2fo10175k. Epub 2012 Jan 5.

Abstract

Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for type 2 diabetes mellitus. In the present study, we investigated whether pharmacologic doses of biotin have the potential to abate insulin resistance in the skeletal muscles of OLETF rats. OLETF rats (34 weeks of age) were divided into 2 groups and given distilled water (OLETF-control group) or distilled water containing 3.3 mg L(-1) of biotin (OLETF-biotin group) for 8 weeks. At the end of experimental period, the OLETF-control rats developed severe hyperglycemia and hyperinsulinemia, whereas the OLETF-biotin rats showed significantly smaller responses to oral glucose tolerance test than the OLETF-control rats. The glucose uptake in the hind limbs of the rats was significantly higher in the OLETF-biotin group than in the OLETF-control group. Biotin administration increased the glucose transporter type 4 (GLUT4) protein content in the total membrane fraction but had little effect on the GLUT4 content in the plasma membrane fraction. These results indicate that administration of a pharmacological dose of biotin prevents the development of insulin resistance in the skeletal muscles of OLETF rats presumably via an increase in GLUT4 protein expression but not via GLUT4 translocation.

摘要

大冢长爪糖尿病肥胖 (OLETF) 大鼠是 2 型糖尿病的动物模型。本研究旨在探讨药理剂量生物素是否具有减轻 OLETF 大鼠骨骼肌胰岛素抵抗的潜力。将 34 周龄的 OLETF 大鼠分为 2 组,分别给予蒸馏水 (OLETF 对照组) 或含 3.3mg/L 生物素的蒸馏水 (OLETF-生物素组)8 周。实验期末,OLETF 对照组大鼠出现严重高血糖和高胰岛素血症,而 OLETF-生物素组大鼠的口服糖耐量试验反应明显小于 OLETF 对照组。OLETF-生物素组大鼠的后肢葡萄糖摄取量明显高于 OLETF 对照组。生物素给药增加了总膜部分的葡萄糖转运蛋白 4 (GLUT4) 蛋白含量,但对质膜部分的 GLUT4 含量影响不大。这些结果表明,药理剂量的生物素给药可通过增加 GLUT4 蛋白表达而不是通过 GLUT4 易位来预防 OLETF 大鼠骨骼肌胰岛素抵抗的发展。

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