Abstract
Oxidative stress represents an impaired metabolic system that promotes damage to cells and tissues. This is the predominant factor that leads to the development and progression of diabetes and diabetic complications. Research has indicated that zinc plays a consequential mechanistic role in the protection against oxidative stress as zinc is required for the proper functioning of the antioxidant system, the suppression of inflammatory mediators, and the modulation of zinc transporters. Recently, the mechanisms surrounding ZnT8, ZIP7, and metallothionein have shown to be of particular pathogenic importance and are considered as potential therapeutic targets in disease management. The literature has shown that zinc dysregulation is associated with diabetes and may be considered as a leading contributor to the deleterious vascular alterations exhibited by the disease. Although further investigation is required, studies have indicated the favorable use of zinc supplementation in the protection against and prevention of oxidative stress and its consequences over the course of the condition. This review aims to provide a comprehensive account of zinc homeostasis, the oxidative mechanisms governed by zinc status, current therapeutic targets, and the impact of zinc supplementation in the prevention of disease onset and in mitigating vascular complications.
Highlights
Diabetes mellitus (DM) is a metabolic disease defined as chronic hyperglycemia caused by insulin resistance (IR) or compromised insulin production [1]
While current literature suggests that ZIP7 may be a contributing factor in the pathogenesis of the risk 2 diabetes mellitus (T2DM), the Zn2+ -mediated mechanisms that are involved in skeletal-muscle glycemic control require further investigation, via in vivo studies of mice and humans
In other cases, the link between the Zn2+ status, glucose metabolism, and IR lacked clarity [12]. While most of these results indicate that Zn2+ supplementation, in Zn2+ -deficient populations, may prevent disruptions of glucose homeostasis, the efficacy of such supplementation remains inconclusive and requires further investigation [14]
Summary
Diabetes mellitus (DM) is a metabolic disease defined as chronic hyperglycemia caused by insulin resistance (IR) or compromised insulin production [1]. The over-production of ROS (superoxide (O2 − ), hydrogen peroxide (H2 O2 ), hydroxyl radicals (·OH), and NADPH-oxidase (NOX)) coupled with reduced antioxidant capacity promotes a pathological imbalance that leads to oxidative stress and inflammation [2,3,4]. Stemming from these alterations, a wide array of diabetic complications is provoked including diabetic nephropathy, neuropathy and retinopathy, as well as the development of cardiovascular diseases (CVDs) [5,6].
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