rising intracellular zinc by membrane depolarization and glucose in insulin-secreting clonal hit-t15 beta cells增加细胞内锌膜去极化和葡萄糖在体内克隆hit-t15β细胞.pdfVIP

Hindawi Publishing Corporation Experimental Diabetes Research Volume 2012, Article ID 190309, 8 pages doi:10.1155/2012/190309 Research Article Rising Intracellular Zinc by Membrane Depolarization and Glucose in Insulin-Secreting Clonal HIT-T15 Beta Cells Kira G. Slepchenko and Yang V. Li Department of Biomedical Sciences, Ohio University Heritage College of Osteopathic Medicine, 346 Irvine Hall, Athens, OH 45701, USA Correspondence should be addressed to Yang V. Li, liy1@ohio.edu Received 19 October 2011; Revised 20 December 2011; Accepted 23 December 2011 Academic Editor: Nils Welsh Copyright © 2012 K. G. Slepchenko and Y. V. Li. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Zinc (Zn2+ ) appears to be intimately involved in insulin metabolism since insulin secretion is correlated with zinc secretion in response to glucose stimulation, but little is known about the regulation of zinc homeostasis in pancreatic beta-cells. This study set out to identify the intracellular zinc transient by imaging free cytosolic zinc in HIT-T15 beta-cells with fluorescent zinc indicators. We observed that membrane depolarization by KCl (30–60 mM) was able to induce a rapid increase in cytosolic concentration of zinc. Multiple zinc transients of similar magnitude were elicited during repeated stimulations. The amplitude of zinc responses was not affected by the removal of extracellular calcium or zinc. However, the half-time of the rising slope was significantly slower after removing extracellular zinc with zinc chelator CaEDTA, suggesting that extracellular zinc affect the initial rising phase of zinc