pubmed-article:20097762 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20097762 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
pubmed-article:20097762 | lifeskim:mentions | umls-concept:C0020663 | lld:lifeskim |
pubmed-article:20097762 | lifeskim:mentions | umls-concept:C0003123 | lld:lifeskim |
pubmed-article:20097762 | lifeskim:mentions | umls-concept:C0033195 | lld:lifeskim |
pubmed-article:20097762 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
pubmed-article:20097762 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
pubmed-article:20097762 | pubmed:issue | 13 | lld:pubmed |
pubmed-article:20097762 | pubmed:dateCreated | 2010-3-22 | lld:pubmed |
pubmed-article:20097762 | pubmed:abstractText | Anorexia and weight loss are prevalent in infectious diseases. To investigate the molecular mechanisms underlying these phenomena, we established animal models of infection-associated anorexia by administrating bacterial and viral products, lipopolysaccharide (LPS) and human immunodeficiency virus-1 transactivator protein (Tat). In these models, we found that the nuclear factor-kappaB (NF-kappaB), a pivotal transcription factor for inflammation-related proteins, was activated in the hypothalamus. In parallel, administration of LPS and Tat increased hypothalamic pro-inflammatory cytokine production, which was abrogated by inhibition of hypothalamic NF-kappaB. In vitro, NF-kappaB activation directly stimulated the transcriptional activity of pro-opiomelanocortin (POMC), a precursor of anorexigenic melanocortin, and mediated the stimulatory effects of LPS, Tat, and pro-inflammatory cytokines on POMC transcription, implying the involvement of NF-kappaB in controlling feeding behavior. Consistently, hypothalamic injection of LPS and Tat caused a significant reduction in food intake and body weight, which was prevented by blockade of NF-kappaB and melanocortin. Furthermore, disruption of I kappaB kinase-beta, an upstream kinase of NF-kappaB, in POMC neurons attenuated LPS- and Tat-induced anorexia. These findings suggest that infection-associated anorexia and weight loss are mediated via NF-kappaB activation in hypothalamic POMC neurons. In addition, hypothalamic NF-kappaB was activated by leptin, an important anorexigenic hormone, and mediates leptin-stimulated POMC transcription, indicating that hypothalamic NF-kappaB also serves as a downstream signaling pathway of leptin. | lld:pubmed |
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pubmed-article:20097762 | pubmed:language | eng | lld:pubmed |
pubmed-article:20097762 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20097762 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20097762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:20097762 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20097762 | pubmed:month | Mar | lld:pubmed |
pubmed-article:20097762 | pubmed:issn | 1083-351X | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KimYoung-BumY... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KarinMichaelM | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:HurMan-WookMW | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:LeeMyung-Shik... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KimMin-SeonMS | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:BaikJa-HyunJH | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KimEun HeeEH | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:LeeKi-UpKU | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:ParkJoong-Yeo... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KimSeung-Whan... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:JangPil-GeumP... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:NamkoongCherl... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KimGeun... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:JeonMin-JaeMJ | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KangGil... | lld:pubmed |
pubmed-article:20097762 | pubmed:author | pubmed-author:KangYeoungsup... | lld:pubmed |
pubmed-article:20097762 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20097762 | pubmed:day | 26 | lld:pubmed |
pubmed-article:20097762 | pubmed:volume | 285 | lld:pubmed |
pubmed-article:20097762 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20097762 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20097762 | pubmed:pagination | 9706-15 | lld:pubmed |
pubmed-article:20097762 | pubmed:dateRevised | 2011-7-27 | lld:pubmed |
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