Differential hypothalamic neuronal activation following peripheral injection of GLP-1 and oxyntomodulin in mice detected by manganese-enhanced magnetic resonance imaging

被引:72
作者
Chaudhri, Owais B.
Parkinson, James R. C.
Kuo, Yu-Ting
Druce, Maralyn R.
Herlihy, Amy H.
Bell, Jimmy D.
Dhillo, Waljit S.
Stanley, Sarah A.
Ghatei, Mohammad A.
Bloom, Stephen R. [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Metab Med, London W12 0NN, England
[2] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, MRC Clin Sci Ctr, Mol Imaging Grp, London W12 0NN, England
[3] Kaohsiung Med Univ, Fac Med, Sch Med, Dept Med Imaging, Kaohsiung, Taiwan
[4] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, MRC Clin Sci Ctr, Imaging Sci Dept,Biol Imaging Ctr, London W12 0NN, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
manganese; Mn2+; MRI; oxyntomodulin; glucagon-like peptide-1; hypothalamus; obesity; gut peptides; appetite; proglucagon;
D O I
10.1016/j.bbrc.2006.09.033
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 anorexigenic gut hormones oxyntomodulin (OXM) and glucagon-like peptide-I (GLP-1) are thought to physiologically regulate appetite and food intake. Using manganese-enhanced magnetic resonance imaging, we have shown distinct patterns of neuronal activation in the hypothalamus in response to intraperitoneal injections into fasted mice of 900 and 5400 nmol/kg OXM or 900 nmol/kg GLP1. Administration of OXM at either dose resulted in a reduced rate of signal enhancement, reflecting a reduction in neuronal activity, in the arcuate, paraventricular, and supraoptic nuclei of the hypothalamus. Conversely, GLP-I caused a reduction in signal enhancement in the paraventricular nucleus only and an increase in the ventromedial hypothalamic nucleus. Our data show that these two apparently similar peptides generate distinct patterns of activation within the hypothalamus, suggesting that GLP-1 and OXM may act via different hypothalamic pathways. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:298 / 306
页数:9
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