Diabetes Care
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 Google Scholar
Google Scholar
Right arrow Articles by Kingston, M. E.
Right arrow Articles by Skoog, W. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kingston, M. E.
Right arrow Articles by Skoog, W. C.
Social Bookmarking
 Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes Care, Vol 9, Issue 3 232-235, Copyright © 1986 by American Diabetes Association


ARTICLES

Maintenance of basal insulin secretion in severe non-insulin-dependent diabetes

ME Kingston and WC Skoog

It has been postulated that glucose regulation is secondary to maintenance of normal basal insulin secretion. Serum glucose, insulin, and C-peptide levels were measured at fasting in 209 consecutive non-insulin-dependent diabetic patients and after glucose stimulation in 193 patients. The basal serum insulin C-peptide levels were not significantly different in control subjects (mean 22 +/- 8.8 microU/ml) and in patients with varying severity of diabetes (mean 24 +/- 9.6 microU/ml) except in the most severely diabetic group [fasting serum glucose greater than 350 mg/dl (19.4 mmol/L), mean 19 +/- 7 microU/ml]. In 39 patients who developed ketonuria without acidosis during follow-up, the mean basal serum insulin was 22 microU/ml during the episode of ketonuria, 21 microU/ml during the glucose tolerance test, and 25 microU/ml after glucose stimulation (statistically nonsignificant differences). Our data suggest that hyperglycemia compensates for beta-cell impairment so that basal insulin secretion usually stays above the threshold for ketoacidosis unless there is marked beta-cell impairment. Patients who fail to increase insulin in response to nutrient challenge are at risk of developing ketosis.
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 © 1986 by the American Diabetes Association.