Free zinc determines the formability of the vesicular dense core in diabetic beta cells

Yi Xian; Mengxuan Zhou; Yuanzhao Hu; Jing Liu; Wenzhen Zhu; Yi Wang

doi:10.1016/j.cellin.2022.100020

Free zinc determines the formability of the vesicular dense core in diabetic beta cells

Cell Insight. 2022 Mar 21;1(2):100020. doi: 10.1016/j.cellin.2022.100020. eCollection 2022 Apr.

Authors

Yi Xian¹, Mengxuan Zhou², Yuanzhao Hu¹, Jing Liu¹, Wenzhen Zhu², Yi Wang³

Affiliations

¹ Peking-Tsinghua Center for Life Sciences, PKU-IDG/McGovern Institute for Brain Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China.
² State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
³ College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China.

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.

Keywords: Beta cell; Dense core; Diabetes; Glucose; Insulin; Zinc.