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Leptin interacts with glucagon‐like peptide‐1 neurons to reduce food intake and body weight in rodents
Author(s) -
Goldstone Anthony P.,
Mercer Julian G.,
Gunn Irene,
Moar Kim M.,
Edwards C.Mark B.,
Rossi Michela,
Howard Jane K.,
Rasheed Shahnawaz,
Turton Mandy D.,
Small Caroline,
Heath Melanie M.,
O'Shea Donal,
Steere Joanna,
Meeran Karim,
Ghatei Mohammed A.,
Hoggard Nigel,
Bloom Stephen R.
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)01103-4
Subject(s) - leptin , medicine , endocrinology , leptin receptor , food intake , neuropeptide , adipose tissue , glucagon like peptide 1 , receptor , neuropeptide y receptor , hormone , chemistry , solitary tract , glucagon , gene isoform , biology , antagonist , obesity , diabetes mellitus , biochemistry , type 2 diabetes , gene
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.