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


     

Am J Physiol Endocrinol Metab 279: E956-E962, 2000;
0193-1849/00 $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 (27)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Persson, K.
Right arrow Articles by Ahrén, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Persson, K.
Right arrow Articles by Ahrén, B.
Vol. 279, Issue 5, E956-E962, November 2000

Reduced GLP-1 and insulin responses and glucose intolerance after gastric glucose in GRP receptor-deleted mice

Kristin Persson1, Ronald L. Gingerich2, Sonali Nayak2, Keiji Wada3, Etsuko Wada3, and Bo Ahrén1

1 Department of Medicine, Lund University, Malmö, SE-205 02 Sweden; 2 Linco Research, St. Charles, Missouri 63301; 3 Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan

By applying a newly developed ELISA technique for determining biologically active intact glucagon-like peptide [GLP-1, GLP-1-(7-36)amide] in mouse, plasma baseline GLP-1 in normal NMRI mice was found to be normally distributed (4.5 ± 0.3 pmol/l; n = 72). In anesthetized mice, gastric glucose (50 or 150 mg) increased plasma GLP-1 levels two- to threefold (P < 0.01). The simultaneous increase in plasma insulin correlated to the 10-min GLP-1 levels (r = 0.36, P < 0.001; n = 12). C57BL/6J mice deleted of the gastrin-releasing peptide (GRP) receptor by genetic targeting had impaired glucose tolerance (P = 0.030) and reduced early (10 min) insulin response (P = 0.044) to gastric glucose compared with wild-type controls. Also, the GLP-1 response to gastric glucose was significantly lower in the GRP receptor-deleted mice than in the controls (P = 0.045). In conclusion, this study has shown that 1) plasma levels of intact GLP-1 increase dose dependently on gastric glucose challenge in correlation with increased insulin levels in mice, and 2) intact GRP receptors are required for normal GLP-1 and insulin responses and glucose tolerance after gastric glucose in mice.

insulin secretion; glucose tolerance; knockout mice; glucagon-like peptide; gastrin-releasing peptide


This article has been cited by other articles:


Home page
 Pharmacol. Rev.Home page
R. T. Jensen, J. F. Battey, E. R. Spindel, and R. V. Benya
International Union of Pharmacology. LXVIII. Mammalian Bombesin Receptors: Nomenclature, Distribution, Pharmacology, Signaling, and Functions in Normal and Disease States
Pharmacol. Rev., March 1, 2008; 60(1): 1 - 42.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
G. E. Lim and P. L. Brubaker
Glucagon-Like Peptide 1 Secretion by the L-Cell: The View From Within
Diabetes, December 1, 2006; 55(Supplement_2): S70 - S77.
[Abstract] [Full Text] [PDF]

Home page
 Ann. N. Y. Acad. Sci.Home page
P. L. BRUBAKER
The Glucagon-Like Peptides: Pleiotropic Regulators of Nutrient Homeostasis
Ann. N.Y. Acad. Sci., July 1, 2006; 1070(1): 10 - 26.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
Y. Anini and P. L. Brubaker
Role of Leptin in the Regulation of Glucagon-Like Peptide-1 Secretion
Diabetes, February 1, 2003; 52(2): 252 - 259.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
M. Nakazaki, A. Crane, M. Hu, V. Seghers, S. Ullrich, L. Aguilar-Bryan, and J. Bryan
cAMP-Activated Protein Kinase-Independent Potentiation of Insulin Secretion by cAMP Is Impaired in SUR1 Null Islets
Diabetes, December 1, 2002; 51(12): 3440 - 3449.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
B. Ahrén and J. J. Holst
The Cephalic Insulin Response to Meal Ingestion in Humans Is Dependent on Both Cholinergic and Noncholinergic Mechanisms and Is Important for Postprandial Glycemia
Diabetes, May 1, 2001; 50(5): 1030 - 1038.
[Abstract] [Full Text]


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