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- Title
Zinc as a paracrine effector in pancreatic islet cell death.
- Authors
Kim, Byoung-Joon; Kim, Yun-Hee; Kim, Sunshin; Kim, Jong-Won; Koh, Jae-Young; Oh, Seung-Hoon; Lee, Moon-Kyu; Kim, Kwang-Won; Lee, Myung-Shik; Kim, B J; Kim, Y H; Kim, S; Kim, J W; Koh, J Y; Oh, S H; Lee, M K; Kim, K W; Lee, M S
- Abstract
Because of a huge amount of Zn2+ in secretory granules of pancreatic islet beta-cells, Zn2+ released in certain conditions might affect the function or survival of islet cells. We studied potential paracrine effects of endogenous Zn2+ on beta-cell death. Zn2+ induced insulinoma/islet cell death in a dose-dependent manner. Chelation of released endogenous Zn2+ by CaEDTA significantly decreased streptozotocin (STZ)-induced islet cell death in an in vitro culture system simulating in vivo circumstances but not in the conventional culture system. Zn2+ chelation in vivo by continuous CaEDTA infusion significantly decreased the incidence of diabetes after STZ administration. N-(6-methoxy-quinolyl)-para-toluene-sulfonamide staining revealed that Zn2+ was densely deposited in degenerating islet cells 24 h after STZ treatment, which was decreased by CaEDTA infusion. We show here that Zn2+ is not a passive element for insulin storage but an active participant in islet cell death in certain conditions, which in time might contribute to the development of diabetes in aged people.
- Subjects
ISLANDS of Langerhans; PHYSIOLOGICAL effects of zinc; PARACRINE mechanisms
- Publication
Diabetes, 2000, Vol 49, Issue 3, p367
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diabetes.49.3.367