Implications of impaired zinc homeostasis in diabetic cardiomyopathy and nephropathy. (27th August 2017)

• Record Type: Journal Article
• Authors: Giacconi, Robertina; Cai, Lu; Costarelli, Laura; Cardelli, Maurizio; Malavolta, Marco; Piacenza, Francesco; Provinciali, Mauro
• Is Part Of: BioFactors. Volume 43:Number 6(2017:Nov./Dec.)
• Page Start: 770
• Page End: 784
• Publication Date: 2017-08-27
• Subjects: zinc -- metallothioneins -- zinc transporters -- diabetes -- diabetic complications; Vitamins -- Physiological effect -- Periodicals; Trace elements -- Physiological effect -- Periodicals; Growth factors -- Physiological effect -- Periodicals; Plant growth promoting substances -- Physiological effect -- Periodicals; Biochemistry -- Periodicals; Nutritional Physiological Phenomena -- Periodicals; Trace Elements -- metabolism -- Periodicals; Vitamins -- metabolism -- Periodicals; Molecular Biology -- Periodicals; 612.399
• DOI: 10.1002/biof.1386
• Languages: English
• ISSNs: 0951-6433

Abstract

Abstract: Impaired zinc homeostasis is observed in diabetes mellitus (DM2) and its complications. Zinc has a specific role in pancreatic β‐cells via insulin synthesis, storage, and secretion. Intracellular zinc homeostasis is tightly controlled by zinc transporters (ZnT and Zip families) and metallothioneins (MT) which modulate the uptake, storage, and distribution of zinc. Several investigations in animal models demonstrate the protective role of MT in DM2 and its cardiovascular or renal complications, while a copious literature shows that a common polymorphism (R325W) in ZnT8, which affects the protein's zinc transport activity, is associated with increased DM2 risk. Emerging studies highlight a role of other zinc transporters in β‐cell function, suggesting that targeting them could make a possible contribution in managing the hyperglycemia in diabetic patients. This article summarizes the current findings concerning the role of zinc homeostasis in DM2 pathogenesis and development of diabetic cardiomyopathy and nephropathy and suggests novel therapeutic targets. © 2017 BioFactors, 43(6):770–784, 2017