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Mesenteric adipose tissue alterations resulting from experimental reactivated colitis

Authors

  • Alessandra Gambero PhD,

    Corresponding author
    1. Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP, Brazil
    • Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Av. São Francisco de Assis 218, 12916-900, Bragança Paulista, SP, Brazil
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  • Marta Maróstica,

    1. Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP, Brazil
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  • Mario José Abdalla Saad MD, PhD,

    1. Department of Internal Medicine, Faculty of Medical Sciences, State University of Campinas, Campinas, SP, Brazil
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  • José Pedrazzoli Jr. MD, PhD

    1. Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP, Brazil
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Abstract

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)

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