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Genetically determined exercise capacity affects systemic glucose response to insulin in rats
Physiological Genomics ( IF 2.5 ) Pub Date : 2021-07-23 , DOI: 10.1152/physiolgenomics.00014.2021
Michael Schwarzer 1 , Annika Molis 1 , Christina Schenkl 1 , Andrea Schrepper 1 , Steven L Britton 2, 3 , Lauren G Koch 4 , Torsten Doenst 1
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Introduction: Aerobic exercise capacity is inversely related to morbidity and mortality as well as to insulin resistance. However, exercising in patients has led to conflicting results, presumably because aerobic exercise capacity consists of intrinsic (genetically determined) and extrinsic (environmentally determined) parts. The contribution of both parts to insulin sensitivity is also not clear. We investigated sedentary and exercised (aerobic interval training) high (HCR) and low capacity runners (LCR) differing in their genetically determined aerobic exercise capacity to determine the contribution of both parts to insulin sensitivity. Methods and Results: LCR and HCR differed in their untrained exercise capacity and body weight. Sedentary LCR displayed a diabetic phenotype with higher random glucose, lower glucose infusion rate during hyperinsulinemic euglycemic clamping than HCR. Echocardiography showed equal morphological and functional parameters and no change with exercise. Four weeks of exercise caused significant improvements in aerobic exercise capacity, which was more pronounced in LCR. However, with respect to glucose use, exercise affected HCR only. In these animals, exercise increased 2-deoxyglucose uptake in gastrocnemius (+58.5 %, p= 0.1) and in epididymal fat (+106 %; p<0.05). Citrate synthase activity also increased in these tissues (gastrocnemius 69 % epididymal fat 63 %). Conclusion: In our model of HCR and LCR, genetic predisposition for low exercise capacity is associated with impaired insulin sensitivity and impedes exercise-induced improvements in insulin response. Our results suggest that genetic predisposition for low aerobic exercise capacity impairs insulin response, which may not be overcome by exercise.

中文翻译:

遗传决定的运动能力影响大鼠全身葡萄糖对胰岛素的反应

简介:有氧运动能力与发病率和死亡率以及胰岛素抵抗呈负相关。然而,在患者身上锻炼导致了相互矛盾的结果,大概是因为有氧运动能力由内在(基因决定)和外在(环境决定)部分组成。这两个部分对胰岛素敏感性的贡献也不清楚。我们调查了久坐和运动(有氧间歇训练)高(HCR)和低容量跑步者(LCR)在基因决定的有氧运动能力方面的差异,以确定这两个部分对胰岛素敏感性的贡献。方法和结果:LCR 和 HCR 在未经训练的运动能力和体重方面存在差异。久坐不动的 LCR 表现出具有较高随机葡萄糖的糖尿病表型,高胰岛素正常血糖钳制期间的葡萄糖输注率低于 HCR。超声心动图显示相同的形态和功能参数,并且不随运动而改变。四周的运动导致有氧运动能力显着提高,这在 LCR 中更为明显。然而,就葡萄糖的使用而言,运动仅影响 HCR。在这些动物中,运动增加了腓肠肌(+58.5%,p=0.1)和附睾脂肪(+106%;p<0.05)对 2-脱氧葡萄糖的摄取。这些组织中的柠檬酸合酶活性也增加了(腓肠肌 69 % 附睾脂肪 63 %)。结论:在我们的 HCR 和 LCR 模型中,低运动能力的遗传易感性与胰岛素敏感性受损有关,并阻碍运动引起的胰岛素反应改善。
更新日期:2021-07-24
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