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 Meyer, H. U.
Right arrow Articles by Felber, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meyer, H. U.
Right arrow Articles by Felber, J. 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 29, Issue 9 752-756, Copyright © 1980 by American Diabetes Association


ARTICLES

Modifications of glucose storage and oxidation in nonobese diabetics, measured by continuous indirect calorimetry

HU Meyer, B Curchod, E Maeder, P Pahud, E Jequier and JP Felber

A new application of continuous indirect calorimetry is described for measuring the disposal of a glucose load. In a group of 10 normal subjects, 3 h after a 100 g oral glucose load, 20 g glucose was oxidized at basal rate, 19 g in response to the load and 63 g stored, while a decrease of 2 g was observed in the glucose space (GS). In a group of four type I, insulin-dependent diabetics, both glucose oxidation (9 g at the basal rate and 4 g in response to the load) and glucose storage (9 g) were markedly decreased, with the remainder either being lost in the urine (36 g) or remaining in the glucose space (42 g). In a group of eight nonobese type II, non-insulin-dependent diabetics, glucose oxidation both in the basal rate and in response to the load was slightly decreased (13 and 14 g, respectively) and glucose storage decreased to 40 g. These results suggest that, in type I diabetics, complete insulin deficiency seriously impairs two major mechanisms regulating glucose homeostasis, i.e., glucose storage and oxidation, while, in type II diabetics, the remaining insulin secretion attentuates these disturbances.
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
J. Clin. Endocrinol. Metab.Home page
I. Kowalska, M. Straczkowski, A. Adamska, A. Nikolajuk, M. Karczewska-Kupczewska, E. Otziomek, and M. Gorska
Serum Retinol Binding Protein 4 Is Related to Insulin Resistance and Nonoxidative Glucose Metabolism in Lean and Obese Women with Normal Glucose Tolerance
J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2786 - 2789.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
F. N. Lee, L. Zhang, D. Zheng, W. S. Choi, and J. H. Youn
Insulin suppresses PDK-4 expression in skeletal muscle independently of plasma FFA
Am J Physiol Endocrinol Metab, July 1, 2004; 287(1): E69 - E74.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1980 by the American Diabetes Association.