Abstract
The adipose tissue hormone, leptin, and the neuropeptide glucagon-like peptide-1 (7-36) amide (GLP-1) both reduce food intake and body weight in rodents. Using dual in situ hybridization, long isoform leptin receptor (OB-Rb) was localized to GLP-1 neurons originating in the nucleus of the solitary tract. ICV injection of the specific GLP-1 receptor antagonist, exendin(9-39), at the onset of dark phase, did not affect feeding in saline pre-treated controls, but blocked the reduction in food intake and body weight of leptin pre-treated rats. These findings suggest that GLP-1 neurons are a potential target for leptin in its control of feeding.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Body Weight / drug effects
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Carrier Proteins / genetics
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Carrier Proteins / metabolism
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DNA Probes
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Eating* / drug effects
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Gene Expression
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Glucagon / analysis
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Glucagon / genetics
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Glucagon / metabolism*
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Glucagon-Like Peptide 1
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In Situ Hybridization
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Leptin
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Light
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Male
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Mice
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Mice, Inbred Strains
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Neurons / chemistry
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Neurons / metabolism*
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Peptide Fragments / metabolism*
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Peptide Fragments / pharmacology
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Proglucagon
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Protein Precursors / analysis
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Protein Precursors / genetics
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Protein Precursors / metabolism*
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Proteins / antagonists & inhibitors
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Proteins / metabolism*
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Proteins / pharmacology
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RNA, Messenger / analysis
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Rats
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Rats, Wistar
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Receptors, Cell Surface*
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Receptors, Leptin
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Solitary Nucleus / cytology*
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Solitary Nucleus / metabolism
Substances
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Carrier Proteins
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DNA Probes
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Leptin
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Peptide Fragments
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Protein Precursors
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Proteins
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RNA, Messenger
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Receptors, Cell Surface
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Receptors, Leptin
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leptin receptor, mouse
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exendin (9-39)
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Proglucagon
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Glucagon-Like Peptide 1
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Glucagon