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


     


Am J Physiol Endocrinol Metab 240: E566-E572, 1981;
0193-1849/81 $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 Cox, J. E.
Right arrow Articles by Powley, T. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cox, J. E.
Right arrow Articles by Powley, T. L.

AJP - Endocrinology and Metabolism, Vol 240, Issue 5 566-E572, Copyright © 1981 by American Physiological Society


ARTICLES

Intragastric pair feeding fails to prevent VMH obesity or hyperinsulinemia

J. E. Cox and T. L. Powley

Female rats with electrolytic lesions of the ventromedial hypothalamus (VMH) were pair fed with controls in a new paradigm in which food was delivered in normal temporal patterns, i.e., those of nonlesioned rats bar pressing for food. Lesions were produced after 6 days of adaptation to this regimen, and the experiment continued for 30 days postlesion. When they were killed, VMH rats contained substantially more carcass lipid than controls (20.4 vs. 12.4%) and were hyperinsulinemic (67.2 vs. 27.6 microunits/ml). Because these elevations developed in the absence of even minor disturbances in feeding patterns, these results support the view that VMH damage confers an essential metabolic bias favoring obesity. Separate VMH groups pair fed exclusively by either oral or intragastric routes exhibited virtually identical exaggerations in fat accumulation (18.4 and 17.7 g above controls, respectively) and plasma insulin (69.2 and 65.4 microunits/ml, respectively). Thus, contrary to a prediction of one form of Powley's (Powley, T. L. Psychol. Rev. 84:89-126, 1977) cephalic phase hypothesis, oropharyngeal stimulation and, hence, the cephalic responses of digestion are not critical for the metabolic disturbances that follow VMH damage.


This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
G. N. Wade
Regulation of body fat content?
Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2004; 286(1): R14 - R15.
[Full Text] [PDF]




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