Postexercise improvement in insulin-stimulated glucose uptake occurs concomitant with greater AS160 phosphorylation in muscle from normal and insulin-resistant rats.
Postexercise improvement in insulin-stimulated glucose uptake occurs concomitant with greater AS160 phosphorylation in muscle from normal and insulin-resistant rats.
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作者：
Castorena CM;Arias EB;Sharma N;Cartee GD
早期对胰岛素敏感性正常的大鼠进行的研究表明，剧烈运动会增加胰岛素刺激的葡萄糖摄取 (GU)，同时 160 kDa (pAS160) 的 Akt 底物 (pAS160) 会发生更大的磷酸化。由于运动对胰岛素抵抗肌肉中 GU 的影响机制尚不清楚，我们的主要目标是评估急性运动（一次）和久坐大鼠喂食饲料（低脂饮食 [LFD]；正常胰岛素敏感性）或高脂肪饮食（HFD；持续 2 周，胰岛素抵抗）。运动后 3 小时 (3hPEX)，分离的滑车上肌用于胰岛素刺激的 GU 和胰岛素信号传导测量。尽管运动并没有增强两组的近端信号传导，但在两个饮食组中，3hPEX 时胰岛素刺激的 GU 超过了各自的久坐对照受试者（久坐）。此外，LFD-3hPEX 的胰岛素刺激 GU 大于 HFD-3hPEX 值。对于 HFD-3hPEX 肌肉，pAS160 超过 HFD-久坐大鼠，但在 LFD-3hPEX 大鼠的肌肉中，pAS160 仍大于 HFD-3hPEX 值。这些结果表明 pAS160 是每个饮食组中运动引起的胰岛素刺激 GU 升高的潜在决定因素，并且还表明 pAS160 可能是胰岛素敏感组与胰岛素抵抗组中胰岛素刺激肌肉运动后 GU 增加的可能调节因素。
Earlier research on rats with normal insulin sensitivity demonstrated that acute exercise increased insulin-stimulated glucose uptake (GU) concomitant with greater phosphorylation of Akt substrate of 160 kDa (pAS160). Because mechanisms for exercise effects on GU in insulin-resistant muscle are unknown, our primary objective was to assess insulin-stimulated GU, proximal insulin signaling (insulin receptor [IR] tyrosine phosphorylation, IR substrate 1–phosphatidylinositol-3-kinase, and Akt phosphorylation and activity), and pAS160 in muscles from acutely exercised (one session) and sedentary rats fed either chow (low-fat diet [LFD]; normal insulin sensitivity) or a high-fat diet (HFD; for 2 weeks, insulin-resistant). At 3 h postexercise (3hPEX), isolated epitrochlearis muscles were used for insulin-stimulated GU and insulin signaling measurements. Although exercise did not enhance proximal signaling in either group, insulin-stimulated GU at 3hPEX exceeded respective sedentary control subjects (Sedentary) in both diet groups. Furthermore, insulin-stimulated GU for LFD-3hPEX was greater than HFD-3hPEX values. For HFD-3hPEX muscles, pAS160 exceeded HFD-Sedentary, but in muscle from LFD-3hPEX rats, pAS160 was greater still than HFD-3hPEX values. These results implicated pAS160 as a potential determinant of the exercise-induced elevation in insulin-stimulated GU for each diet group and also revealed pAS160 as a possible mediator of greater postexercise GU of insulin-stimulated muscles from the insulin-sensitive versus insulin-resistant group.
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Lee YS;Li P;Huh JY;Hwang IJ;Lu M;Kim JI;Ham M;Talukdar S;Chen A;Lu WJ;Bandyopadhyay GK;Schwendener R;Olefsky J;Kim JB
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