AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 259: R45-R52, 1990;
0363-6119/90 $5.00
This Article
Right arrow Full Text (PDF)
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Harris, R. B.
Right arrow Articles by Martin, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Harris, R. B.
Right arrow Articles by Martin, R. J.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 259, Issue 1 45-R52, Copyright © 1990 by American Physiological Society


ARTICLES

Site of action of putative lipostatic factor: food intake and peripheral pentose shunt activity

R. B. Harris and R. J. Martin
Department of Foods and Nutrition, University of Georgia, Athens 30602.

Obesity due to overfeeding in one parabiotic rat results in mild hypophagia and specific loss of fat from its partner. Studies were conducted to determine whether the changes in body composition were reversible and whether the nonsignificant reduction in food intake was a primary response to a humoral lipostatic factor. Tube feeding partners of overfed rats 0.5 g more food per day than eaten voluntarily prevented loss of fat, although hepatic and adipose glucose-6-phosphate dehydrogenase activities were depressed. Glucose flux through the pentose phosphate pathway was inhibited in both adipose and hepatic tissue from thin partners of obese rats, although fatty acid synthesis was depressed only in adipose tissue. Response to insulin by adipocytes from ad libitum partners of obese rats appeared to be blunted, but insulin sensitivity was normal. When overfeeding stopped, both partners returned to control body composition, suggesting that the changes observed in parabiotic partners of obese rats were physiological responses to a putative circulating lipostatic factor rather than a nonspecific consequence of parabiosis.


This article has been cited by other articles:


Home page
FASEB J.Home page
G. FRUHBECK and J. GOMEZ-AMBROSI
Rationale for the existence of additional adipostatic hormones
FASEB J, September 1, 2001; 15(11): 1996 - 2006.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online