Inflammatory alterations in mesenteric adipose tissue in Crohn's disease

P Desreumaux, O Ernst, K Geboes, L Gambiez… - Gastroenterology, 1999 - Elsevier
P Desreumaux, O Ernst, K Geboes, L Gambiez, D Berrebi, H Müller-Alouf, S Hafraoui…
Gastroenterology, 1999Elsevier
Background & Aims: Abnormalities of fat in the mesentery including adipose tissue
hypertrophy and fat wrapping have been long recognized on surgical specimens as
characteristic features of Crohn's disease. However, the importance, origin, and significance
of the mesenteric fat hypertrophy in this chronic inflammatory disease are unknown.
Peroxisome proliferator–activated receptor γ (PPARγ) is a crucial factor involved in the
homeostasis of adipose tissue, a major source of biologically active mediators. Methods …
Background & Aims
Abnormalities of fat in the mesentery including adipose tissue hypertrophy and fat wrapping have been long recognized on surgical specimens as characteristic features of Crohn's disease. However, the importance, origin, and significance of the mesenteric fat hypertrophy in this chronic inflammatory disease are unknown. Peroxisome proliferator–activated receptor γ (PPARγ) is a crucial factor involved in the homeostasis of adipose tissue, a major source of biologically active mediators.
Methods
Intra-abdominal fat accumulation was quantified using a magnetic resonance imaging method in patients with Crohn's disease and controls. PPARγ and inflammatory cytokines synthesized by mesenteric adipose tissues were assessed by quantitative polymerase chain reaction, in situ hybridization, and immunohistochemistry.
Results
In vivo, patients with Crohn's disease have an important accumulation of intra-abdominal fat. This mesenteric obesity, present from the onset of the disease, is associated with overexpression of PPARγ and tumor necrosis factor (TNF)-α, synthesized, at least in part, by adipocytes.
Conclusions
These results suggest that confined increased PPARγ mesenteric concentrations could lead to the mesenteric fat hypertrophy, which could actively participate through the synthesis of TNF-α in the inflammatory response. GASTROENTEROLOGY 1999;117:73-81
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