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Combination of Metformin and Exercise in Management of Metabolic Abnormalities Observed in Type 2 Diabetes Mellitus
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy ( IF 3.3 ) Pub Date : 2021-09-16 , DOI: 10.2147/dmso.s328694 Filip Jevtovic 1
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy ( IF 3.3 ) Pub Date : 2021-09-16 , DOI: 10.2147/dmso.s328694 Filip Jevtovic 1
Affiliation
Abstract: Excess nutrient intake and lack of exercise characterize the problem of obesity and are common factors in insulin resistance (IR). With an increasing number of prediabetic, and type 2 diabetic populations, metformin is still the most prescribed glucose-lowering drug and is often accompanied by recommendations for regular physical exercise. Metformin, by the inhibition of complex 1 of the electron transport chain, and exercise, by increasing energy expenditure, both elicit a low cellular energy state that leads to improvements in glucose control via activation of adenosine 5ʹ monophosphate-activated protein kinase (AMPK). An augmented stimulation of the energy-sensing enzyme AMPK by either of the two modalities leads to an increase in glycogenolysis, glucose uptake, fat oxidation, a decrease in glycogen and protein synthesis, and gluconeogenesis in muscle and the liver, which are remarked as having positive effects on metabolic pathophysiology observed in IR and type 2 diabetes mellitus (T2DM). While both modalities exploit the energy-sensing enzyme AMPK to attain glucose homeostasis, the synergistic effect of these two treatments is not distinctly supported by the literature. Further, an antagonistic dynamic has been observed in cases where metformin and exercise were combined. Reduction of insulin-sensitizing effects of exercise and an overall hindrance of exercise performance and adaptations have been reported and could suggest the possible incongruity of these two modalities. The aim of this review is to elucidate the effect that metformin and exercise have on the management of the metabolic abnormalities observed in T2DM and to provide an insight into the interaction of these two modalities.
Keywords: exercise, metformin, glucose control, type 2 diabetes mellitus, AMPK
中文翻译:
二甲双胍和运动联合治疗 2 型糖尿病中观察到的代谢异常
摘要:过量的营养摄入和缺乏运动是肥胖问题的特征,也是胰岛素抵抗 (IR) 的常见因素。随着糖尿病前期和 2 型糖尿病人群数量的增加,二甲双胍仍然是处方最多的降糖药物,并且通常伴随着定期体育锻炼的建议。二甲双胍通过抑制电子传递链的复合物 1 和运动(通过增加能量消耗)引起低细胞能量状态,从而通过激活腺苷 5' 单磷酸激活蛋白激酶 (AMPK) 来改善葡萄糖控制。两种方式中任何一种对能量感应酶 AMPK 的增强刺激都会导致糖原分解、葡萄糖摄取、脂肪氧化增加,糖原和蛋白质合成减少,肌肉和肝脏中的糖异生,被认为对 IR 和 2 型糖尿病 (T2DM) 中观察到的代谢病理生理学具有积极影响。虽然这两种方式都利用能量感应酶 AMPK 来实现葡萄糖稳态,但这两种治疗的协同作用并未得到文献的明确支持。此外,在二甲双胍和运动相结合的情况下,已经观察到拮抗作用。据报道,运动的胰岛素敏化作用降低以及运动表现和适应的整体障碍,这可能表明这两种方式可能不协调。
关键词:运动,二甲双胍,血糖控制,2型糖尿病,AMPK
更新日期:2021-09-16
Keywords: exercise, metformin, glucose control, type 2 diabetes mellitus, AMPK
中文翻译:
二甲双胍和运动联合治疗 2 型糖尿病中观察到的代谢异常
摘要:过量的营养摄入和缺乏运动是肥胖问题的特征,也是胰岛素抵抗 (IR) 的常见因素。随着糖尿病前期和 2 型糖尿病人群数量的增加,二甲双胍仍然是处方最多的降糖药物,并且通常伴随着定期体育锻炼的建议。二甲双胍通过抑制电子传递链的复合物 1 和运动(通过增加能量消耗)引起低细胞能量状态,从而通过激活腺苷 5' 单磷酸激活蛋白激酶 (AMPK) 来改善葡萄糖控制。两种方式中任何一种对能量感应酶 AMPK 的增强刺激都会导致糖原分解、葡萄糖摄取、脂肪氧化增加,糖原和蛋白质合成减少,肌肉和肝脏中的糖异生,被认为对 IR 和 2 型糖尿病 (T2DM) 中观察到的代谢病理生理学具有积极影响。虽然这两种方式都利用能量感应酶 AMPK 来实现葡萄糖稳态,但这两种治疗的协同作用并未得到文献的明确支持。此外,在二甲双胍和运动相结合的情况下,已经观察到拮抗作用。据报道,运动的胰岛素敏化作用降低以及运动表现和适应的整体障碍,这可能表明这两种方式可能不协调。
关键词:运动,二甲双胍,血糖控制,2型糖尿病,AMPK