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


     

This Article
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schade, D. S.
Right arrow Articles by Eaton, R. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schade, D. S.
Right arrow Articles by Eaton, R. P.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 26, Issue 6 596-599, Copyright © 1977 by American Diabetes Association

ARTICLES

The controversy concerning counterregulatory hormone secretion. A hypothesis for the prevention of diabetic ketoacidosis?

DS Schade and RP Eaton

Diabetic ketoacidosis is characterized by an excess secretion of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Experimental evidence obtained in both diabetic man and animals suggests that elevation of the plasma concentration of these hormones is necessary to initiate excess hepatic production of ketone bodies. This increase in hepatic ketogenesis in concert with inability of peripheral tissues to completely utilize ketone bodies results in clinical ketoacidosis. This hypothesis would suggest that pharmacologic control of excess counterregulatory hormone secretion would be a rational therapeutic modality to prevent diabetic ketoacidosis.
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?


This article has been cited by other articles:


Home page
 DiabetesHome page
Y. Liu, Y. Nakagawa, Y. Wang, R. Sakurai, P. V. Tripathi, K. Lutfy, and T. C. Friedman
Increased Glucocorticoid Receptor and 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression in Hepatocytes May Contribute to the Phenotype of Type 2 Diabetes in db/db Mice
Diabetes, January 1, 2005; 54(1): 32 - 40.
[Abstract] [Full Text] [PDF]

Home page
 Postgrad. Med. J.Home page
V Rosival
Failure to develop diabetic ketoacidosis in a newly presenting type 1 diabetic patient
Postgrad. Med. J., May 1, 2002; 78(919): 317 - 317.
[Full Text] [PDF]

Home page
 Arch Intern MedHome page
E. A. Warner, G. S. Greene, M. S. Buchsbaum, D. S. Cooper, and B. E. Robinson
Diabetic Ketoacidosis Associated With Cocaine Use
Arch Intern Med, September 14, 1998; 158(16): 1799 - 1802.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1977 by the American Diabetes Association.