Abstract
During the progression of type 2 diabetes, total body zinc deficiency disrupts the formability of the electron-dense core in beta-cell vesicles, but the mechanism is unclear. Using fluorescence imaging, transmission electron microscopy and pharmacokinetics assays, we established a strong link between an increasing concentration of free zinc and the formability enhancement of the dense core electron density. Thus, our results highlight a mechanism by which zinc supplementation enhances the maturation of dense cores and restores the secretion of insulin in two diabetic mouse models both in vitro and in vivo. This study provides a potential research direction for investigating the etiology and nutrition of zinc in the management of type 2 diabetes.