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Submitted on October 29, 2004
Accepted on March 1, 2005
Department of Research (P.L., D.S., H.Z., U.K., B.M.), Department of Endocrinology, Diabetology and Clinical Nutrition (H.Z., U.K., B.M.), University Hospital, CH-4031 Basel, Switzerland
* To whom correspondence should be addressed. E-mail: Philippe.Linscheid{at}unibas.ch.
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 in 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-1
and LPS-challenged mesenchymal stem cell (MSC)-derived adipocytes, but not in undifferentiated MSC. In contrast, ADM expression occurred before and after adipogenic differentiation. IFN
co-administration inhibited IL-1-mediated ProCT and CGRP secretion by 78% and 34%, respectively, but augmented IL-1-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, TNF
and IL-1 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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interferon- •
endotoxin
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