Gambero Alessandra, Maróstica Marta, Abdalla Saad Mario José, Pedrazzoli José
Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP, Brazil.
Inflamm Bowel Dis. 2007 Nov;13(11):1357-64. doi: 10.1002/ibd.20222.
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.
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.
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-gamma-2 expression, and higher basal lipolysis and TNF-alpha production when compared to normal rats. Perinodal mesenteric adipocytes present normal diameters, downregulated levels of PPAR-gamma-2, higher basal lipolysis and TNF-alpha, and leptin and adiponectin production.
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.
脂肪组织分泌大量激素，这些激素可在局部或远处发挥作用，调节免疫反应、炎症以及许多内分泌和代谢功能。肠系膜脂肪异常在手术标本中一直被认为是克罗恩病的特征性表现；然而，其在慢性炎症性疾病中的重要性尚不清楚。此外，包裹淋巴结或其他密集淋巴组织团块的脂肪库中的脂肪细胞具有许多位点特异性生理特性。
在本研究中，评估了通过反复向结肠内注入三硝基苯磺酸诱导的实验性结肠炎期间肠系膜和结周肠系膜脂肪组织的变化，重点关注形态和活性改变以及脂肪细胞因子产生情况。
经过35天的实验方案后，尽管结肠炎动物体重较低，但肠系膜脂肪量更大。还评估了另一个脂肪组织库，附睾脂肪组织，未观察到其质量变化。与正常大鼠相比，结肠炎动物的肠系膜脂肪细胞直径减小，PPAR-γ-2表达正常，基础脂解和TNF-α产生增加。结周肠系膜脂肪细胞直径正常，PPAR-γ-2水平下调，基础脂解和TNF-α、瘦素及脂联素产生增加。
研究结果表明，肠系膜脂肪组织在实验性炎症期间具有位点特异性反应，其中结周脂肪组织保留产生不同脂肪细胞因子的能力。这些物质可能在许多淋巴结方面产生干扰，而肠系膜脂肪组织产生的物质可能直接导致炎症过程加重。
