Aerobic Exercise and Metformin: A Dual Approach to Enhancing Glycemic Maintenance in Type 2 Diabetes Mellitus.

Chonnam medical journal Pub Date : 2025-01-01 Epub Date: 2025-01-24 DOI:10.4068/cmj.2025.61.1.9
Zahra Eslami, Gholamreza Roshandel, Seyed Javad Mirghani
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Abstract

Type 2 diabetes mellitus (T2DM) is a widespread metabolic condition characterized by elevated glucose levels followed by deficiency in insulin secretion. Metformin notably decreased the incidence of T2DM by 31% and it exerts its effects through various signaling pathways. Databases searched included PubMed, Google Scholar, and Scopus from 2000 to 2024. One of the primary mechanisms involves AMPK activation which causes reduced lipogenesis and improved fatty acid oxidation in the liver and muscles. Key molecules affected by metformin include acetyl-CoA carboxylase (ACC) and sterol regulatory element-binding protein 1c (SREBP-1c), both involved in lipid synthesis regulation. Aerobic exercise has also emerged as a crucial component in managing T2DM due to its improved effects on hyperglycemia and insulin sensitivity. Key signaling pathways affected in T2DM include the PI3K/Akt, AMP-activated protein kinase (AMPK), and MAPK/ERK pathways which play essential roles in regulating glucose homeostasis, glycogenesis, and insulin secretion. When comparing the mechanisms and efficacy of aerobic exercise and metformin, it becomes evident that aerobic exercise primarily enhances physical fitness and metabolic function, while metformin exerts its effects through biochemical pathways involving AMPK activation. Aerobic exercise and metformin are effective for managing T2DM, though they operate through different mechanisms. Regular aerobic exercise improves insulin sensitivity, enhances cardiovascular health, and promotes weight loss, while metformin primarily decreases hepatic gluconeogenesis and enhances insulin secretion. Understanding the intricate signaling pathways affected by metformin and aerobic exercise provides valuable insights into its mechanisms of action and clinical implications for treating diabetic patients effectively.

有氧运动和二甲双胍:促进2型糖尿病患者血糖维持的双重途径。
2型糖尿病(T2DM)是一种广泛存在的代谢疾病,其特征是葡萄糖水平升高,随后是胰岛素分泌不足。二甲双胍可显著降低T2DM发病率31%,并通过多种信号通路发挥作用。检索的数据库包括2000年至2024年的PubMed、b谷歌Scholar和Scopus。其中一个主要机制涉及AMPK的激活,它导致肝脏和肌肉中的脂肪生成减少和脂肪酸氧化改善。二甲双胍影响的关键分子包括乙酰辅酶a羧化酶(ACC)和甾醇调节元件结合蛋白1c (SREBP-1c),它们都参与脂质合成调节。由于有氧运动对高血糖和胰岛素敏感性的改善作用,它也成为控制2型糖尿病的重要组成部分。受T2DM影响的关键信号通路包括PI3K/Akt、amp活化蛋白激酶(AMPK)和MAPK/ERK通路,它们在调节葡萄糖稳态、糖生成和胰岛素分泌中发挥重要作用。通过对比有氧运动和二甲双胍的作用机制和效果,我们发现有氧运动主要是增强体质和代谢功能,而二甲双胍则是通过激活AMPK等生化途径发挥作用。有氧运动和二甲双胍对控制2型糖尿病有效,尽管它们通过不同的机制起作用。有规律的有氧运动可以改善胰岛素敏感性,促进心血管健康,促进体重减轻,而二甲双胍主要是降低肝脏糖异生,促进胰岛素分泌。了解二甲双胍和有氧运动影响的复杂信号通路,为其作用机制和有效治疗糖尿病患者的临床意义提供了宝贵的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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