Mesenteric adipose tissue alterations resulting from experimental reactivated colitis
Article first published online: 29 JUN 2007
Copyright © 2007 Crohn's & Colitis Foundation of America, Inc.
Inflammatory Bowel Diseases
Volume 13, Issue 11, pages 1357–1364, November 2007
How to Cite
Gambero, A., Maróstica, M., Abdalla Saad, M. J. and Pedrazzoli, J. (2007), Mesenteric adipose tissue alterations resulting from experimental reactivated colitis. Inflamm Bowel Dis, 13: 1357–1364. doi: 10.1002/ibd.20222
- Issue published online: 3 OCT 2007
- Article first published online: 29 JUN 2007
- Manuscript Accepted: 25 MAY 2007
- Manuscript Received: 30 NOV 2006
- FAPESP = Fundação de Amparo à Pesquisa do Estado de São Paulo
- perinodal adipose tissue;
- mesenteric adipose tissue
Background: Adipose tissue secretes a large number of hormones that act either locally or at distant sites, modulating immune responses, inflammation, and many endocrine and metabolic functions. Abnormalities of fat in the mesentery have been long recognized in surgical specimens as characteristic features of Crohn's disease; however, the importance of this in chronic inflammatory disease is unknown. Additionally, adipocytes in depots that enclose lymph nodes or other dense masses of lymphoid tissue have many site-specific physiological properties.
Methods: In this study, the alterations of mesenteric and perinodal mesenteric adipose tissue during experimental colitis, induced by repeated intracolonic trinitrobenzene sulfonic acid instillations, were evaluated, focusing on morphological and activity alterations and the adipocytokine production profile.
Results: After a 35-day protocol, the colitis animals presented greater mesenteric fat masses despite their lower body weights. Another adipose tissue depot, epididymal adipose tissue, was also evaluated and no change in mass was observed. The mesenteric adipocyte from colitis animals had a reduced diameter, normal PPAR-γ-2 expression, and higher basal lipolysis and TNF-α production when compared to normal rats. Perinodal mesenteric adipocytes present normal diameters, downregulated levels of PPAR-γ-2, higher basal lipolysis and TNF-α, and leptin and adiponectin production.
Conclusions: The findings suggest that mesenteric adipose tissue has a site-specific response during experimental inflammation, where perinodal adipose tissue retains the ability to produce different adipocytokines. These substances may interfere in many lymph node aspects, while mesenteric adipose tissue produces substances that could contribute directly to aggravate the inflammatory process.
(Inflamm Bowel Dis 2007)