Inflammatory alterations in mesenteric adipose tissue in Crohn's disease
- P Desreumaux 1, O Ernst , K Geboes , L Gambiez , D Berrebi , H Müller-Alouf , S Hafraoui , D Emilie , N Ectors , M Peuchmaur , A Cortot , M Capron , J Auwerx , J F Colombel
- P Desreumaux 1, O Ernst , K Geboes
- 1Laboratoire de Recherche sur les Maladies Inflammatoires Intestinales (CRI 4U004B), Centre Hospitalier Universitaire (CHU), Lille, France.
- 0Laboratoire de Recherche sur les Maladies Inflammatoires Intestinales (CRI 4U004B), Centre Hospitalier Universitaire (CHU), Lille, France.
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View abstract on PubMed
Summary
This summary is machine-generated.Crohn's disease patients exhibit increased mesenteric fat due to higher PPARgamma levels, potentially driving inflammation via TNF-alpha production. This mesenteric obesity is a key feature from the disease's start.
Area Of Science
- Gastroenterology and Immunology
- Adipose Tissue Biology
Background
- Mesenteric fat abnormalities, including hypertrophy and wrapping, are recognized features of Crohn's disease (CD).
- The role and origin of mesenteric fat hypertrophy in CD pathogenesis remain unclear.
- Peroxisome proliferator-activated receptor gamma (PPARgamma) is vital for adipose tissue homeostasis and mediator production.
Purpose Of The Study
- To investigate the significance and origin of mesenteric fat hypertrophy in Crohn's disease.
- To explore the role of PPARgamma and inflammatory cytokines in mesenteric adipose tissue of CD patients.
Main Methods
- Quantified intra-abdominal fat using magnetic resonance imaging (MRI) in CD patients and controls.
- Assessed PPARgamma and inflammatory cytokine expression in mesenteric adipose tissue via quantitative PCR, in situ hybridization, and immunohistochemistry.
Main Results
- CD patients showed significant intra-abdominal fat accumulation (mesenteric obesity) from the disease's onset.
- Mesenteric obesity in CD was associated with overexpression of PPARgamma and tumor necrosis factor (TNF)-alpha.
- Adipocytes were identified as a source of PPARgamma and TNF-alpha synthesis.
Conclusions
- Increased PPARgamma concentrations in mesenteric fat may cause hypertrophy in CD.
- Mesenteric fat hypertrophy, through TNF-alpha synthesis, may actively contribute to the inflammatory response in CD.
- Targeting PPARgamma in mesenteric adipose tissue could be a therapeutic strategy for Crohn's disease.
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