Unraveling Quercetin's Potential: A Comprehensive Review of Its Properties and Mechanisms of Action, in Diabetes and Obesity Complications

被引:1
作者
Yi, Ruhan [1 ]
Liu, Yun [1 ]
Zhang, Xu [1 ]
Sun, Xiance [2 ]
Wang, Ningning [1 ]
Zhang, Cong [1 ]
Deng, Haoyuan [1 ]
Yao, Xiaofeng [2 ]
Wang, Shaopeng [3 ]
Yang, Guang [1 ]
机构
[1] Dalian Med Univ, Dept Food Nutr & Safety, Dalian, Peoples R China
[2] Dalian Med Univ, Dept Occupat & Environm Hlth, Dalian, Peoples R China
[3] Dalian Med Univ, Affiliated Hosp 1, Dept Cardiol, Dalian, Peoples R China
基金
中国国家自然科学基金;
关键词
hypoglycemic; insulin resistance; quercetin; T2DM; INSULIN-RESISTANCE; OXIDATIVE STRESS; SKELETAL-MUSCLE; GENE-EXPRESSION; INFLAMMATION; LIVER; ACID; RATS; HOMEOSTASIS; METABOLISM;
D O I
10.1002/ptr.8332
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The prevalence of diabetes is escalating alarmingly, placing a significant economic burden on the global healthcare system. The use of chemical substances extracted from plants has been demonstrated to be an effective method for the treatment and control of insulin resistance and Type 2 diabetes mellitus (T2DM). New research indicates that natural phytochemicals present in fruits and vegetables are expected to become drugs for the treatment of diabetes and the prevention of related complications. Quercetin, a widely distributed flavonoid, is well-known for its antioxidant, anti-inflammatory, anticancer, and antidiabetic properties. This article provides a comprehensive account of the mechanism of action of quercetin on diabetes and obesity complications in vivo and in vitro. It elucidates the impact of quercetin on various cells. These include hepatocytes, renal cells, skeletal muscle cells, and adipocytes. Furthermore, this article discusses the mechanism of quercetin on organ damage in diabetic mice induced by STZ, alloxan, diet, and spontaneous Type 2 diabetic mice caused by genetic defects. Additionally, it addresses the pharmacokinetics of quercetin and its potential for synergistic effects with existing diabetic drugs.
引用
收藏
页码:5641 / 5656
页数:16
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