Glucose intolerance but normal satiety in mice with a null mutation in the glucagon–like peptide 1 receptor gene
Glucagon–like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversial. The regulation of nutrient–induced insulin secretion is dependent on the secretion of incretins, gut–derived peptides that...
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| Published in | Nature medicine Vol. 2; no. 11; pp. 1254 - 1258 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.11.1996
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Glucagon–like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversial. The regulation of nutrient–induced insulin secretion is dependent on the secretion of incretins, gut–derived peptides that potentiate insulin secretion from the pancreatic islets
1
. To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene (
GLP1R
). These
GLP1R
−/−
mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild–type mice but not in
GLP1R
−/−
mice; however, no evidence for abnormal body weight or feeding behavior was observed in
GLP1R
−/−
mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity
in vivo
. |
|---|---|
| AbstractList | Glucagon-like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversal. The regulation of nutrient-induced insulin secretion is dependent on the secretion of incretins, gut-derived peptides that potentiate insulin secretion from the pancreatic islets. To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene (GLP1R). These GLP1R-/- mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild-type mice but not in GLP1R-/- mice; however, no evidence for abnormal body weight or feeding behavior was observed in GLP1R-/- mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo.Glucagon-like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversal. The regulation of nutrient-induced insulin secretion is dependent on the secretion of incretins, gut-derived peptides that potentiate insulin secretion from the pancreatic islets. To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene (GLP1R). These GLP1R-/- mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild-type mice but not in GLP1R-/- mice; however, no evidence for abnormal body weight or feeding behavior was observed in GLP1R-/- mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo. Glucagon-like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversal. The regulation of nutrient-induced insulin secretion is dependent on the secretion of incretins, gut-derived peptides that potentiate insulin secretion from the pancreatic islets. To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene (GLP1R). These GLP1R-/- mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild-type mice but not in GLP1R-/- mice; however, no evidence for abnormal body weight or feeding behavior was observed in GLP1R-/- mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo. Glucagon-like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversial. The regulation of nutrient-induced insulin secretion is dependent on the secretion of incretins, gut-derived peptides that potentiate insulin secretion from the pancreatic islets. To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene (GLP1R). These GLP1R super(-/-) mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild-type mice but not in GLP1R super(-/-) mice; however, no evidence for abnormal body weight or feeding behavior was observed in GLP1R super(-/-) mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo. Glucagon–like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversial. The regulation of nutrient–induced insulin secretion is dependent on the secretion of incretins, gut–derived peptides that potentiate insulin secretion from the pancreatic islets 1 . To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene ( GLP1R ). These GLP1R −/− mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild–type mice but not in GLP1R −/− mice; however, no evidence for abnormal body weight or feeding behavior was observed in GLP1R −/− mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo . |
| Author | Brubaker, P.L. Brown, T.J. Scrocchi, L.A. Maclusky, N. Drucker, D.J. Auerbach, A.B. Joyner, A.L. |
| Author_xml | – sequence: 1 givenname: L.A. surname: Scrocchi fullname: Scrocchi, L.A. organization: Department of Medicine, University of Toronto, and Banting and Best Diabetes Centre, the Toronto Hospital – sequence: 2 givenname: T.J. surname: Brown fullname: Brown, T.J. organization: Department of Obstetrics and Gynecology, the Toronto Hospital, University of Toronto – sequence: 3 givenname: N. surname: Maclusky fullname: Maclusky, N. organization: Department of Obstetrics and Gynecology, the Toronto Hospital, University of Toronto – sequence: 4 givenname: P.L. surname: Brubaker fullname: Brubaker, P.L. organization: Department of Physiology, University of Toronto – sequence: 5 givenname: A.B. surname: Auerbach fullname: Auerbach, A.B. organization: Departments of Cell Biology, Physiology and Neuroscience, Skirball Institute ofBiomoIecular Medicine, New York University Medical Center – sequence: 6 givenname: A.L. surname: Joyner fullname: Joyner, A.L. organization: Departments of Cell Biology, Physiology and Neuroscience, Skirball Institute ofBiomoIecular Medicine, New York University Medical Center – sequence: 7 givenname: D.J. surname: Drucker fullname: Drucker, D.J. organization: Department of Medicine, University of Toronto, and Banting and Best Diabetes Centre, the Toronto Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/8898756$$D View this record in MEDLINE/PubMed |
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| Snippet | Glucagon–like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide... Glucagon-like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide... |
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| SubjectTerms | Animals Biomedical and Life Sciences Biomedicine Blood Glucose - analysis Cancer Research Female Gene Deletion Glucagon - pharmacology Glucagon-Like Peptide 1 Glucagon-Like Peptide-1 Receptor Glucose - metabolism Glucose - pharmacology Glucose Intolerance Infectious Diseases Insulin - blood Male Metabolic Diseases Mice Molecular Medicine Neurosciences Peptide Fragments - pharmacology Protein Precursors - pharmacology Rats Receptors, Glucagon - genetics Receptors, Glucagon - metabolism |
| Title | Glucose intolerance but normal satiety in mice with a null mutation in the glucagon–like peptide 1 receptor gene |
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