| pubmed-article:18506089 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0020663 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0027895 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0061355 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C2350345 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:18506089 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:18506089 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:18506089 | pubmed:dateCreated | 2008-10-29 | lld:pubmed |
| pubmed-article:18506089 | pubmed:abstractText | Intracerebroventricular (icv) administration of glucagon-like peptide-1 (GLP-1) inhibits food intake and induces c-fos expression in the hypothalamus. However, the effects of GLP-1 on hypothalamic neuronal activity or neuropeptide mRNA expression are unknown. In this study, we examined the effects of GLP-1 on fasting-induced changes in the expression of hypothalamic orexigenic and anorexigenic neuropeptide. Food intake was significantly inhibited after icv injection of GLP-1 in 48 h fasted rats. Hypothalamic neuropeptide Y (NPY) and agouti-related peptide (AgRP) mRNAs were significantly increased by fasting, whereas icv GLP-1 treatment significantly attenuated these fasting-induced increases. Both proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels were decreased by fasting, while GLP-1 treatment attenuated fasting-induced decreases in POMC and CART expression. We also determined the mRNA levels of AMP-activated kinase (AMPK) and found that fasting resulted in a significant stimulation of hypothalamic AMPKalpha2 mRNA. Fasting-induced increase in AMPKalpha2 mRNA was almost completely prevented by GLP-1 treatment. Analysis of phosphorylated AMPKalpha and acetyl CoA carboxylase showed similar results. Taken together, our observation suggests that the decreased food intake by GLP-1 is caused by preventing the fasting-induced increase in hypothalamic NPY and AgRP and the fasting-induced decrease in hypothalamic POMC and CART. Our results also suggest that the food intake lowering effect of GLP-1 is caused by reversing the fasting-induced increase in hypothalamic AMPK activity. Therefore we conclude that the anorectic effect of GLP-1 seems to be mediated by, at least in part, by the hypothalamus. | lld:pubmed |
| pubmed-article:18506089 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18506089 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18506089 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18506089 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18506089 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18506089 | pubmed:issn | 1348-4540 | lld:pubmed |
| pubmed-article:18506089 | pubmed:author | pubmed-author:FangZZ | lld:pubmed |
| pubmed-article:18506089 | pubmed:author | pubmed-author:ParkSeungjoon... | lld:pubmed |
| pubmed-article:18506089 | pubmed:author | pubmed-author:ChungHyunjuH | lld:pubmed |
| pubmed-article:18506089 | pubmed:author | pubmed-author:SeoSangheeS | lld:pubmed |
| pubmed-article:18506089 | pubmed:author | pubmed-author:JuSungheeS | lld:pubmed |
| pubmed-article:18506089 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18506089 | pubmed:volume | 55 | lld:pubmed |
| pubmed-article:18506089 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18506089 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18506089 | pubmed:pagination | 867-74 | lld:pubmed |
| pubmed-article:18506089 | pubmed:meshHeading | pubmed-meshheading:18506089... | lld:pubmed |
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| pubmed-article:18506089 | pubmed:meshHeading | pubmed-meshheading:18506089... | lld:pubmed |
| pubmed-article:18506089 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18506089 | pubmed:articleTitle | Acute effects of glucagon-like peptide-1 on hypothalamic neuropeptide and AMP activated kinase expression in fasted rats. | lld:pubmed |
| pubmed-article:18506089 | pubmed:affiliation | Department of Pharmacology, Biomedical Science Institute and Medical Research Center for Reactive Oxygen Species, Kyunghee University School of Medicine, Seoul, Korea. | lld:pubmed |
| pubmed-article:18506089 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18506089 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18506089 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18506089 | lld:pubmed |
