AJP - GI Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 234: G20-G24, 1978;
0193-1857/78 $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 Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ritter, R.
Right arrow Articles by Balch, O.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Ritter, R.
Right arrow Articles by Balch, O.
AJP: Gastrointestinal and Liver Physiology, Vol 234, Issue 1, G20-G24
Copyright © 1978 by American Physiological Society

ARTICLES

Feeding in response to insulin but not to 2-deoxy-D-glucose in the hamster

RC Ritter and OK Balch

Adult hamsters did not increase their food intake in response to subcutaneous injection of 2-deoxy-D-glucose (2DG) at doses of 50, 200, 350, 500, 750, 1,000, or 1,500 mg/kg. The failure to feed in response to 2DG was apparent regardless of time of testing and length of test. Hamsters did display marked hyperglycemia after 2DG treatment. Therefore, hamsters do detect and form neural responses to 2DG. In contrast to 2DG, injection of regular insulin, 2, 4, or 8 U/animal, caused hamsters to significantly increase their food intake over a 5-h test period. Furthermore, injection of 4 U of protamine zinc insulin twice daily also caused pronounced increases in food intake and weight gain by hamsters. Because hamsters do not seem to posses a feeding response to 2DG-induced glucoprivation, it seems unlikely that insulin elicits feeding via the glucoprivic control in this species. The results suggest that 1) hamsters lack the glucoprivic control of feeding behavior as exercised by 2DG, 2) 2DG and insulin treatments are not equivalent ingestive challenges, and 3) insulin-induced feeding may result in part from activation of a nonglucoprivic control of food intake.





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