Muscle-Specific Ablation of Glucose Transporter 1 (GLUT1) Does Not Impair Basal or Overload-Stimulated Skeletal Muscle Glucose Uptake.
Muscle-Specific Ablation of Glucose Transporter 1 (GLUT1) Does Not Impair Basal or Overload-Stimulated Skeletal Muscle Glucose Uptake.
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DOI：
10.3390/biom12121734
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发表时间：
2022-11-23
期刊：
影响因子：
5.5
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中科院分区：
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葡萄糖转运蛋白1(GLUT1)被认为只介导骨骼肌基础(胰岛素非依赖性)葡萄糖摄取；然而最近的研究表明，机械超负荷，一种抵抗运动训练的模型，增加了肌肉GLUT1的水平。这项研究的主要目的是确定GLUT1是否对基础或超负荷刺激的肌肉葡萄糖摄取是必需的。建立肌肉特异性GLUT1基因敲除小鼠(MGLUT1KO)，检测体重、体成分、代谢、全身葡萄糖调节、肌肉葡萄糖转运蛋白和肌肉[~(3 H)]-2-脱氧葡萄糖摄取的变化。在表达GLUT1-6或GLUT10的HEK293细胞中也检测到[~3H]-己糖摄取±Bay-876。MGLUT1KO小鼠在体重、瘦体重、全身代谢、葡萄糖耐量、基础或超负荷刺激的肌肉葡萄糖摄取方面没有损害。胰岛素反应性GLUT4没有补偿作用。在mGLUT1KO小鼠肌肉中，超负荷刺激机械敏感性GLUT6的高表达，但不能刺激GLUT3或GLUT10的表达。在对照组和mGLUT1KO小鼠肌肉中，0.05µM Bay-876可抑制超负荷刺激的葡萄糖摄取，但不影响基础葡萄糖摄取。在GLUT-HEK293细胞中，Bay-876通过GLUT1、GLUT3、GLUT4、GLUT6和GLUT10抑制葡萄糖摄取。综上所述，这些发现表明GLUT1不介导基础肌肉葡萄糖摄取，并提示一种新的葡萄糖转运机制介导超负荷刺激的葡萄糖摄取。
Glucose transporter 1 (GLUT1) is believed to solely mediate basal (insulin-independent) glucose uptake in skeletal muscle; yet recent work has demonstrated that mechanical overload, a model of resistance exercise training, increases muscle GLUT1 levels. The primary objective of this study was to determine if GLUT1 is necessary for basal or overload-stimulated muscle glucose uptake. Muscle-specific GLUT1 knockout (mGLUT1KO) mice were generated and examined for changes in body weight, body composition, metabolism, systemic glucose regulation, muscle glucose transporters, and muscle [3H]-2-deoxyglucose uptake ± the GLUT1 inhibitor BAY-876. [3H]-hexose uptake ± BAY-876 was also examined in HEK293 cells-expressing GLUT1-6 or GLUT10. mGLUT1KO mice exhibited no impairments in body weight, lean mass, whole body metabolism, glucose tolerance, basal or overload-stimulated muscle glucose uptake. There was no compensation by the insulin-responsive GLUT4. In mGLUT1KO mouse muscles, overload stimulated higher expression of mechanosensitive GLUT6, but not GLUT3 or GLUT10. In control and mGLUT1KO mouse muscles, 0.05 µM BAY-876 impaired overload-stimulated, but not basal glucose uptake. In the GLUT-HEK293 cells, BAY-876 inhibited glucose uptake via GLUT1, GLUT3, GLUT4, GLUT6, and GLUT10. Collectively, these findings demonstrate that GLUT1 does not mediate basal muscle glucose uptake and suggest that a novel glucose transport mechanism mediates overload-stimulated glucose uptake.
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