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

Administration of biotin prevents the development of insulin resistance in the skeletal muscles of Otsuka Long-Evans Tokushima fatty rats
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DOI:
10.1039/c2fo10175k
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发表时间:
2012-04-01
期刊:
影响因子:
6.1
通讯作者:
Furukawa, Yuji
Furukawa, Yuji
中科院分区:
农林科学1区
文献类型:
--
作者:
Sasaki, Yuka;Sone, Hideyuki;Furukawa, Yuji

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大冢Long-Evans德岛脂肪(OLETF)大鼠是2型糖尿病的动物模型。在本研究中,我们研究了药物剂量的生物素是否有可能减轻OLETF大鼠骨骼肌的胰岛素抵抗。34周龄的OLETF大鼠分为2组,分别给予蒸馏水(OLETF对照组)或含有3.3 mg L-1生物素的蒸馏水(OLETF生物素组)8周。实验结束时,oletf对照组大鼠出现了严重的高血糖和高胰岛素血症,而oletf生物素组大鼠对口服糖耐量试验的反应明显小于oletf对照组大鼠。oletf生物素组大鼠后肢葡萄糖摄取明显高于oletf对照组。生物素增加了总膜组分中葡萄糖转运蛋白4 (GLUT4)的含量,但对质膜组分中GLUT4的含量影响不大。这些结果表明,给药一定剂量的生物素可以防止OLETF大鼠骨骼肌中胰岛素抵抗的发生,可能是通过增加GLUT4蛋白的表达,而不是通过GLUT4易位。
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.