Insulino-mimetic and anti-diabetic effects of zinc.
Insulino-mimetic and anti-diabetic effects of zinc.
复制标题
DOI：
10.1016/j.jinorgbio.2012.11.006
复制
发表时间：
2013-03
影响因子：
3.9
通讯作者：
George Vardatsikos;N. R. Pandey;A. Srivastava
中科院分区：
文献类型：
--
作者：
George Vardatsikos;N. R. Pandey;A. Srivastava
虽然人们早就知道锌 (Zn) 对于正常生长和维持正常生物功能至关重要，但锌也被证明可以发挥胰岛素模拟和抗糖尿病作用。这些胰岛素样特性已在分离的细胞、组织以及不同的 1 型和 2 型糖尿病动物模型中得到证实。研究发现，锌治疗可以改善糖尿病啮齿动物模型中的碳水化合物和脂质代谢。在分离的细胞中，它增强葡萄糖转运、糖原和脂质合成，并抑制糖异生和脂肪分解。锌化合物产生胰岛素样作用的分子机制涉及胰岛素信号通路几个关键成分的激活，其中包括细胞外信号调节激酶 1/2 (ERK1/2) 和磷脂酰肌醇 3-激酶 (PI3-K)/蛋白激酶 B/Akt (PKB/Akt) 通路。然而，锌触发这些途径激活的精确分子机制仍有待阐明。在这篇综述中，我们简要介绍了锌的历史，概述了其胰岛素模拟和抗糖尿病作用，以及锌发挥这些作用的潜在机制。
While it has long been known that zinc (Zn) is crucial for the proper growth and maintenance of normal biological functions, Zn has also been shown to exert insulin-mimetic and anti-diabetic effects. These insulin-like properties have been demonstrated in isolated cells, tissues, and different animal models of type 1 and type 2 diabetes. Zn treatment has been found to improve carbohydrate and lipid metabolism in rodent models of diabetes. In isolated cells, it enhances glucose transport, glycogen and lipid synthesis, and inhibits gluconeogenesis and lipolysis. The molecular mechanism responsible for the insulin-like effects of Zn compounds involves the activation of several key components of the insulin signaling pathways, which include the extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase (PI3-K)/protein kinase B/Akt (PKB/Akt) pathways. However, the precise molecular mechanisms by which Zn triggers the activation of these pathways remain to be clarified. In this review, we provide a brief history of zinc, and an overview of its insulin-mimetic and anti-diabetic effects, as well as the potential mechanisms by which zinc exerts these effects.