Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Diabetes Publish Ahead of Print published online ahead of print February 22, 2007
DOI: 10.2337/db06-1454
This Article
Right arrow Full Text (PDF)
Right arrow Erratum (v56,p1747)
Right arrow All Versions of this Article:
db06-1454v1
56/4/1107    most recent
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhou, H.
Right arrow Articles by Robertson, R. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhou, H.
Right arrow Articles by Robertson, R. P.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Original Research

Zinc, Not Insulin, Regulates the Rat Alpha Cell Response to Hypoglycemia in vivo

Huarong Zhou1, Tao Zhang1, Jamie S. Harmon1, Joseph Bryan2, and R. Paul Robertson1,,3

1Pacific Northwest Research Institute
2Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX
3Departments of Medicine and Pharmacology at the University of Washington, 720 Broadway, Seattle, WA 98122

The intraislet insulin hypothesis proposes that the decrement in beta cell insulin secretion during hypoglycemia provides an activation signal for alpha cells to release glucagon. A more recent hypothesis proposes that zinc atoms suppress glucagon secretion via their ability to open alpha cell KATP channels. Since insulin binds zinc and zinc is co-secreted with insulin, we tested whether decreased zinc delivery to the alpha cell activates glucagon secretion. In streptozotocin-diabetic Wistar rats, we observed that switching off intrapancreatic artery insulin infusions in vivo during hypoglycemia greatly improved glucagon secretion (control = 240 ± 261; expt'l = 4346 ± 1259; n=5, AUC, pg/ml/90 min, p<0.02). Switching off pancreatic artery infusions of zinc chloride during hypoglycemia also improved the glucagon response (control = 817 ± 107; expt'l = 3445 ± 573; n=6, AUC, pg/ml/90 min, p<0.01). However, switching off zinc-free insulin infusions had no effect. Studies of glucose uptake in muscle and liver cell lines verified that the zinc-free insulin was biologically active. We conclude that zinc atoms, not the insulin molecule itself, provide the switch-off signal from the beta cell to the alpha cell to initiate glucagon secretion during hypoglycemia.


Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2007 by the American Diabetes Association.