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


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Boden, G.
Right arrow Articles by Homko, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Boden, G.
Right arrow Articles by Homko, C.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes 52:133-137, 2003
© 2003 by the American Diabetes Association, Inc.

Effects of Acute Insulin Excess and Deficiency on Gluconeogenesis and Glycogenolysis in Type 1 Diabetes

Guenther Boden, Peter Cheung, and Carol Homko

From the Division of Endocrinology/Diabetes/Metabolism and the General Clinical Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania

To determine whether insulin induces acute changes in endogenous glucose production (EGP) via changes in gluconeogenesis (GNG), glycogenolysis (GL), or both, we measured GNG (with 2H2O) and GL (EGP-GNG) in nine patients with type 1 diabetes during acute insulin excess produced by subcutaneous injection of insulin and during insulin deficiency which developed between 5 and 8 h after insulin injection. During insulin excess, free insulin concentration rose fivefold (from 36 to 180 pmol/l). Plasma glucose was maintained between 6.2 and 6.7 mmol/l for ~4 h with IV glucose. EGP (with 6,6-2H glucose) decreased from 17.1 to 9.8 µmol · kg-1 · min-1 after 1 h. This decrease was almost completely accounted for by a decrease in GL (from 10.7 to 4.6 µmol · kg-1 · min-1). During insulin deficiency, plasma glucose rose from 6.2 to 10.5 mmol/l and EGP from 9.5 to 14.3 µmol/kg min. The increase in EGP again was accounted for by an increase in GL.

We conclude that in type 1 diabetes acute regulation of EGP by insulin is mainly via changes in GL while GNG changes little during the early hours of acute insulin excess or deficiency.


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
P. Kishore, I. Gabriely, M.-H. Cui, J. Di Vito, S. Gajavelli, J.-H. Hwang, and H. Shamoon
Role of Hepatic Glycogen Breakdown in Defective Counterregulation of Hypoglycemia in Intensively Treated Type 1 Diabetes
Diabetes, March 1, 2006; 55(3): 659 - 666.
[Abstract] [Full Text] [PDF]

Home page
 ANN INTERN MEDHome page
G. Boden, K. Sargrad, C. Homko, M. Mozzoli, and T. P. Stein
Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with Type 2 Diabetes
Ann Intern Med, March 15, 2005; 142(6): 403 - 411.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
J. N. Clore, J. S. Stillman, J. Li, S. J. D. O'Keefe, and J. R. Levy
Differential effect of saturated and polyunsaturated fatty acids on hepatic glucose metabolism in humans
Am J Physiol Endocrinol Metab, August 1, 2004; 287(2): E358 - E365.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2003 by the American Diabetes Association.