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Originally published In Press as doi:10.1074/jbc.M009382200 on March 21, 2001

J. Biol. Chem., Vol. 276, Issue 24, 21489-21499, June 15, 2001
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Glucagon-like Peptide (GLP)-2 Action in the Murine Central Nervous System Is Enhanced by Elimination of GLP-1 Receptor Signaling*

Julie LovshinDagger §, Jennifer EstallDagger , Bernardo YustaDagger , Theodore J. Brown, and Daniel J. DruckerDagger ||

From the Dagger  Department of Medicine, Banting and Best Diabetes Centre, Toronto General Hospital, and the  Division of Reproductive Science, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1Y5, and the University of Toronto, Toronto, Ontario M5G 2C4, Canada

Glucagon-like peptide-2 (GLP-2) regulates energy homeostasis via effects on nutrient absorption and maintenance of gut mucosal epithelial integrity. The biological actions of GLP-2 in the central nervous system (CNS) remain poorly understood. We studied the sites of endogenous GLP-2 receptor (GLP-2R) expression, the localization of transgenic LacZ expression under the control of the mouse GLP-2R promoter, and the actions of GLP-2 in the murine CNS. GLP-2R expression was detected in multiple extrahypothalamic regions of the mouse and rat CNS, including cell groups in the cerebellum, medulla, amygdala, hippocampus, dentate gyrus, pons, cerebral cortex, and pituitary. A 1.5-kilobase fragment of the mouse GLP-2R promoter directed LacZ expression to the gastrointestinal tract and CNS regions in the mouse that exhibited endogenous GLP-2R expression, including the cerebellum, amygdala, hippocampus, and dentate gyrus. Intracerebroventricular injection of GLP-2 significantly inhibited food intake during dark-phase feeding in wild-type mice. Disruption of glucagon-like peptide-1 receptor (GLP-1R) signaling with the antagonist exendin-(9-39) in wild-type mice or genetically in GLP-1R-/- mice significantly potentiated the anorectic actions of GLP-2. These findings illustrate that CNS GLP-2R expression is not restricted to hypothalamic nuclei and demonstrate that the anorectic effects of GLP-2 are transient and modulated by the presence or absence of GLP-1R signaling in vivo.

* This work was supported in part by operating grants from the Canadian Institutes of Health Research and the Ontario Research and Development Challenge Fund.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF338223 and AF338224.

§ Recipient of a doctoral research award from the Canadian Institutes of Health Research.

|| Canadian Institutes of Health Research Senior Scientist. To whom correspondence should be addressed: Banting and Best Diabetes Centre, Toronto General Hospital, 101 College St., CCRW3-845, Toronto, Ontario M5G 2C4, Canada. Tel.: 416-340-4125; Fax: 416-978-4108; E-mail: d.drucker@utoronto.ca.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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