| pubmed-article:10510338 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0299583 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0036751 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0243127 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C1157570 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:10510338 | lifeskim:mentions | umls-concept:C0443331 | lld:lifeskim |
| pubmed-article:10510338 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10510338 | pubmed:dateCreated | 1999-11-2 | lld:pubmed |
| pubmed-article:10510338 | pubmed:abstractText | Leptin administration inhibits diencephalic nitric oxide synthase (NOS) activity and increases brain serotonin (5-HT) metabolism in mice. We evaluated food intake, body-weight gain, diencephalic NOS activity, and diencephalic content of tryptophan (TRP), 5-HT, hydroxyindoleacetic acid (5-HIAA), and 5-HIAA/5-HT ratio after intracerebroventricular (ICV) or intraperitoneal (IP) leptin injection in mice. Five consecutive days of ICV or IP leptin injections induced a significant reduction in neuronal NOS (nNOS) activity, and caused a dose-dependent increase of 5-HT, 5-HIAA, and the 5-HIAA/5-HT ratio. Diencephalic 5-HT metabolism showed a significant increase in 5-HT, 5-HIAA, and the 5-HIAA/5-HT ratio 3 hours after a single leptin injection. This effect was maintained for 3 hours and had disappeared by 12 hours after injection. After a single IP leptin injection, the peak for 5-HT, 5-HIAA, and the 5-HIAA/5-HT ratio was achieved at 6 hours. Single injections of ICV or IP leptin significantly increased diencephalic 5-HT content. Leptin-induced 5-HT increase was antagonized by the coadministration of L-arginine only when the latter was ICV injected, whereas D-arginine did not influence leptin effects on brain 5-HT content. Finally, in nNOS-knockout mice, the appetite-suppressant activity of leptin was strongly reduced, and the leptin-induced increase in brain 5-HT metabolism was completely abolished. Our results indicate that the L-arginine/NO pathway is involved in mediating leptin effects on feeding behavior, and demonstrate that nNOS activity is required for the effects of leptin on brain 5-HT turnover. | lld:pubmed |
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| pubmed-article:10510338 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10510338 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10510338 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10510338 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10510338 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10510338 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:CaputiA PAP | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:SautebinLL | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:BuemiMM | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:Di RosaMM | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:CalapaiGG | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:CampoG MGM | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:CoricaFF | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:CorsonelloAA | lld:pubmed |
| pubmed-article:10510338 | pubmed:author | pubmed-author:MauroV NVN | lld:pubmed |
| pubmed-article:10510338 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10510338 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:10510338 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10510338 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10510338 | pubmed:pagination | 975-82 | lld:pubmed |
| pubmed-article:10510338 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:10510338 | pubmed:meshHeading | pubmed-meshheading:10510338... | lld:pubmed |
| pubmed-article:10510338 | pubmed:meshHeading | pubmed-meshheading:10510338... | lld:pubmed |
