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 Google Scholar
Google Scholar
Right arrow Articles by Juhl, C.
Right arrow Articles by Pørksen, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Juhl, C.
Right arrow Articles by Pørksen, N.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Diabetes 51:S255-S257, 2002
© 2002 by the American Diabetes Association, Inc.

Section 6: Pusatile and Phasic Insulin Release in Normal and Diabetic Men

Effects of Fasting on Physiologically Pulsatile Insulin Release in Healthy Humans

Claus Juhl1, Thorbjørn Grøfte1, Peter C. Butler2, Johannes D. Veldhuis3, Ole Schmitz1, and Niels Pørksen1

1 Department of Endocrinology and Metabolism M, Aarhus University Hospital, Aarhus, Denmark
2 Department of Endocrinology and Diabetes, University of Southern California, Los Angeles, CA
3 U.S. Department of Medicine and National Science Foundation Center for Biological Timing, Charlottesville, VA

Insulin is released as secretory bursts superimposed on basal release. The overall contribution of secretory bursts was recently quantified as at least 75%, and the main regulation of insulin secretion is through perturbation of the amount of insulin released and the frequency of these secretory bursts. The mode of delivery of insulin into the circulation seems important for insulin action, and therefore physiological conditions that alter the pattern of insulin release may affect insulin action through this mechanism. To assess the mechanisms by which fasting changes the amount of insulin released and the frequency, amplitude, and overall contribution of pulsatile insulin secretion, we used a validated deconvolution model to examine pulsatile insulin secretion during 10 and 58 h of fasting in seven healthy subjects. The subjects were studied for 75 min before (0–75 min) and 75 min during (115–190 min) a glucose infusion (2.5 mg · kg-1 · min-1). We found that the pulsatile insulin release pattern was preserved and that, at fasting, overall insulin release is adjusted to needs by a reduced amount of insulin released (10.1 ± 1.7 vs. 16.0 ± 3.2 pmol/l/pulse, P < 0.05) but similar frequency (6.3 ± 0.4 vs. 6.1 ± 0.4 min/pulse) of the insulin secretory bursts. In both states, glucose infusion caused an increase (P < 0.05) in amount (100–200%) and frequency (~20%). The impact of increased glucose concentration on pulse frequency seems distinct for in vivo versus in vitro pulsatile insulin secretion and may indicate the presence of a glucose-sensitive pacemaker, which initiates the coordinated secretory bursts. Increased insulin/C-peptide ratio at long-term fasting (6.0 vs. 9.1%, P < 0.01) indicates that the changes in insulin release patterns may be accompanied by changes in hepatic insulin extraction.


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 TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2002 by the American Diabetes Association.