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J. Biol. Chem., Vol. 276, Issue 24, 21489-21499, June 15, 2001
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From the 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 The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF338223 and AF338224.
Glucagon-like Peptide (GLP)-2 Action in the Murine
Central Nervous System Is Enhanced by Elimination of GLP-1 Receptor
Signaling*
§,,,
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
/ 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.
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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