Leptin interacts with glucagon-like peptide-1 neurons to reduce food intake and body weight in rodents

被引:124
作者
Goldstone, AP
Mercer, JG
Gunn, I
Moar, KM
Edwards, CMB
Rossi, M
Howard, JK
Rasheed, S
Turton, MD
Small, C
Heath, MM
OShea, D
Steere, J
Meeran, K
Ghatei, MA
Hoggard, N
Bloom, SR
机构
[1] UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,HAMMERSMITH HOSP,DEPT ENDOCRINOL & METAB MED,LONDON W12 0NN,ENGLAND
[2] ROWETT RES INST,MOL NEUROENDOCRINOL UNIT,ABERDEEN AB21 9SB,SCOTLAND
[3] ROWETT RES INST,MOL PHYSIOL GRP,ABERDEEN AB21 9SB,SCOTLAND
基金
英国惠康基金;
关键词
leptin; GLP-1; exendin(9-39); in situ hybridization; nucleus of the solitary tract; feeding;
D O I
10.1016/S0014-5793(97)01103-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 1997 Federation of European Biochemical Societies.
引用
收藏
页码:134 / 138
页数:5
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