揭示锌、硼、铬和硒在糖尿病发病机制中的复杂作用:综述

Karar Nadhum Jawad Musafer, Hani Ajrina Zulkeflee, Wan Nor Fazila Hafizan Wan Nik, Siti Nadirah Ab Rahim, Tuan Salwani Tuan Ismail
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引用次数: 0

摘要

微量元素是微量营养成分,只需少量,但对人体许多组织的生物功能至关重要。在多种情况下进行的研究发现,糖尿病(DM)与微量元素之间存在着重要联系,而微量元素则是由重叠的细胞代谢系统紊乱引起的。锌、硼、铬和硒的含量过高或过低都会引起细胞代谢的某些改变。这些都会导致 DM 的发生。这些变化包括:1)胰岛素分泌颗粒的有效释放受到干扰;2)促炎细胞因子的产生和氧化应激状态;3)胰岛素信号通路失效;4)葡萄糖转运体下调导致葡萄糖组织吸收减少。胰岛素浓度过高或过低都与胰岛素抵抗的形成有关。然而,相互矛盾的证据使得它们的最佳营养水平难以确定。例如,微量浓度的铅可能会加速胰岛素抵抗的发展。本综述旨在强调 4 种微量元素在新陈代谢中的作用,以及当体内微量元素含量低于最佳水平时,它们对糖尿病发病机制的影响。了解这些微量元素的后果,可为个性化糖尿病管理的治疗可能性和突破性进展铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unraveling the Complex Role of Zinc, Boron, Chromium, and Selenium in the Pathogenesis of Diabetes Mellitus: A Review
Trace elements are micronutrient components that are only required in small amounts but are critical for the biological functions of many human body tissues. Studies in multiple settings found significant connections between diabetic mellitus (DM) and trace elements caused by disturbances of overlapping cellular metabolic systems. Zinc, boron, chromium, and selenium at either extremely high or low levels could elicit some alteration in cellular metabolism. These lead to the development of DM. The changes include 1) the disturbance in the efficient release of insulin secretory granules, 2) the production of proinflammatory cytokines and oxidative stress state, 3) the failure of insulin signalling pathway, and 4) the reduction of glucose tissue uptake secondary to the downregulation of glucose transporters. Both significantly high and low concentrations have been linked to the development of insulin resistance. Nevertheless, conflicting evidence makes their optimum nutritional levels difficult to establish. For example, lead at a trace concentration may accelerate the development of insulin resistance. The purpose of this review is to emphasise the metabolic role of the 4 trace elements and their influence on the pathogenesis of diabetes when body levels are below optimal. Understanding the consequences of these elements could pave the way for therapeutic possibilities and breakthroughs in personalised DM management.
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