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Papers In Press, published online ahead of print March 21, 2001
Department of Medicine, Toronto General Hospital, Toronto, Ontario M5G2C4
Corresponding Author: d.drucker{at}utoronto.ca
Glucagon-like peptide-2 (GLP-2) is expressed in gut endocrine cells where it regulates energy homeostasis via effects on nutrient absorption, and maintenance of 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 biological 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-kilo base-pair 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 wildtype mice. Disruption of glucagon-like peptide-1 (GLP-1) receptor signaling with the antagonist exendin (9-39) in wildtype mice, or genetically in GLP-1 receptor -/- 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-1 receptor signaling in vivo.
J. Biol. Chem, 10.1074/jbc.M009382200
Submitted on October 13, 2000
Revised on March 19, 2001
Accepted on March 20, 2001
Glucagon-like peptide-2 action in the murine central nervous system is enhanced by elimination of GLP-1 receptor signaling
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