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
Affiliations
Yi Xian
Peking-Tsinghua Center for Life Sciences, PKU-IDG/McGovern Institute for Brain Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China
Mengxuan Zhou
State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking University, Beijing, 100871, China
Yuanzhao Hu
Peking-Tsinghua Center for Life Sciences, PKU-IDG/McGovern Institute for Brain Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China
Jing Liu
Peking-Tsinghua Center for Life Sciences, PKU-IDG/McGovern Institute for Brain Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China
Wenzhen Zhu
State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking University, Beijing, 100871, China
Yi Wang
Corresponding author.; College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China
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.
