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 278: R1518-R1523, 2000;
0363-6119/00 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wildman, H. F.
Right arrow Articles by Smith, G. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wildman, H. F.
Right arrow Articles by Smith, G. P.
Vol. 278, Issue 6, R1518-R1523, June 2000

Effects of leptin and cholecystokinin in rats with a null mutation of the leptin receptor Leprfak

H. F. Wildman1, S. Chua Jr.2, R. L. Leibel2, and G. P. Smith1

1 E. W. Bourne Laboratory, Department of Psychiatry, Joan and Sanford I. Weill Medical College of Cornell University, and the New York-Presbyterian Hospital, Westchester Division, White Plains 10605, and 2 Department of Pediatrics, Division of Molecular Genetics, Columbia University College of Physicians and Surgeons, New York, New York 10032

The Koletsky ("corpulent") obese rat is homozygous for an autosomal recessive mutation of the leptin receptor (Lepr) that results in hyperphagia, obesity, and hyperlipidemia. Unlike the Lepr mutation that characterizes the fatty Zucker rat (Leprfa), the Koletsky mutation (Leprfak) is null. Because the Leprfak mutation is null, exogenous leptin should have no effect on body weight or food intake in fak/fak rats. We confirmed that prediction: murine leptin, administered into the third ventricle for 5 consecutive days, did not affect daily food intake or body weight in fak/fak rats but produced dose-related inhibitions of food intake and body weight in +/+ and +/fak rats. Although fak/fak rats did not respond to leptin, their response to CCK-8 (4 µg/kg ip) injected before 30-min test meals of 10% sucrose was not different from that of +/+ or +/fak rats. These results demonstrate that the fak/fak rat is a good model in which to analyze the controls of food intake, energy expenditure, and energy storage in the absence of leptin effects.

food intake; satiation; body weight; genetic obesity; sucrose


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
W. A. Cupples
Regulation of body weight
Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2002; 282(5): R1264 - R1266.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
G. F. DiBona
Neuropeptide Y
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2002; 282(3): R635 - R636.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
J. J. Hwa, L. Ghibaudi, J. Gao, and E. M. Parker
Central melanocortin system modulates energy intake and expenditure of obese and lean Zucker rats
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2001; 281(2): R444 - R451.
[Abstract] [Full Text] [PDF]


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