Source:http://linkedlifedata.com/resource/pubmed/id/15761041
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2005-5-17
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pubmed:abstractText |
Human adipose tissue is a contributor to inflammation- and sepsis-induced elevation of serum procalcitonin (ProCT). Several calcitonin (CT) peptides, including ProCT, CT gene-related peptide (CGRP), and adrenomedullin (ADM) are suspected mediators in human inflammatory diseases. Therefore, we aimed to explore the expression, interactions, and potential roles of adipocyte-derived CT peptide production. Expression of CT peptide-specific transcripts was analyzed by RT-PCR and quantitative real-time PCR in human adipose tissue biopsies and three different inflammation-challenged human adipocyte models. ProCT, CGRP, and ADM secretions were assessed by immunological methods. Adipocyte transcriptional activity, glycerol release, and insulin-mediated glucose transport were studied after exogenous CGRP and ADM exposure. With the exception of amylin, CT peptides were expressed in adipose tissue biopsies from septic patients, inflammation-activated mature explanted adipocytes, and macrophage-activated preadipocyte-derived adipocytes. ProCT and CGRP productions were significantly augmented in IL-1beta and lipopolysaccharide-challenged mesenchymal stem cell-derived adipocytes but not in undifferentiated mesenchymal stem cells. In contrast, ADM expression occurred before and after adipogenic differentiation. Interferon-gamma coadministration inhibited IL-1beta-mediated ProCT and CGRP secretion by 78 and 34%, respectively but augmented IL-1beta-mediated ADM secretion by 50%. Exogenous CGRP and ADM administration induced CT, CGRP I, and CGRP II mRNAs and dose-dependently (10(-10) and 10(-6) m) enhanced glycerol release. In contrast, no CGRP- and ADM-mediated effects were noted on ADM, TNFalpha, and IL-1beta mRNA abundances. In summary, CGRP and ADM are two differentially regulated novel adipose tissue secretion factors exerting autocrine/paracrine roles. Their lipolytic effect (glycerol release) suggests a metabolic role in adipocytes during inflammation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
146
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2699-708
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15761041-Adipocytes,
pubmed-meshheading:15761041-Adipose Tissue,
pubmed-meshheading:15761041-Adrenomedullin,
pubmed-meshheading:15761041-Autocrine Communication,
pubmed-meshheading:15761041-Calcitonin Gene-Related Peptide,
pubmed-meshheading:15761041-Cells, Cultured,
pubmed-meshheading:15761041-Coculture Techniques,
pubmed-meshheading:15761041-Gene Expression Regulation,
pubmed-meshheading:15761041-Humans,
pubmed-meshheading:15761041-Macrophages,
pubmed-meshheading:15761041-Paracrine Communication,
pubmed-meshheading:15761041-Peptides,
pubmed-meshheading:15761041-RNA, Messenger,
pubmed-meshheading:15761041-Sepsis
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pubmed:year |
2005
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pubmed:articleTitle |
Autocrine/paracrine role of inflammation-mediated calcitonin gene-related peptide and adrenomedullin expression in human adipose tissue.
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pubmed:affiliation |
Department of Research, University Hospitals, Hebelstrasse 20, 4031 Basel, Switzerland. philippe.linscheid@unibas.ch
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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