Desreumaux P, Ernst O, Geboes K, Gambiez L, Berrebi D, Müller-Alouf H, Hafraoui S, Emilie D, Ectors N, Peuchmaur M, Cortot A, Capron M, Auwerx J, Colombel J F
Laboratoire de Recherche sur les Maladies Inflammatoires Intestinales (CRI 4U004B), Centre Hospitalier Universitaire (CHU), Lille, France.
Gastroenterology. 1999 Jul;117(1):73-81. doi: 10.1016/s0016-5085(99)70552-4.
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 gamma (PPARgamma) is a crucial factor involved in the homeostasis of adipose tissue, a major source of biologically active mediators.
Intra-abdominal fat accumulation was quantified using a magnetic resonance imaging method in patients with Crohn's disease and controls. PPARgamma and inflammatory cytokines synthesized by mesenteric adipose tissues were assessed by quantitative polymerase chain reaction, in situ hybridization, and immunohistochemistry.
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 PPARgamma and tumor necrosis factor (TNF)-alpha, synthesized, at least in part, by adipocytes.
These results suggest that confined increased PPARgamma mesenteric concentrations could lead to the mesenteric fat hypertrophy, which could actively participate through the synthesis of TNF-alpha in the inflammatory response.
肠系膜脂肪异常,包括脂肪组织肥大和脂肪包裹,长期以来在手术标本中被视为克罗恩病的特征性表现。然而,这种慢性炎症性疾病中肠系膜脂肪肥大的重要性、起源及意义尚不清楚。过氧化物酶体增殖物激活受体γ(PPARγ)是参与脂肪组织稳态的关键因子,脂肪组织是生物活性介质的主要来源。
采用磁共振成像方法对克罗恩病患者和对照组的腹腔内脂肪堆积情况进行量化。通过定量聚合酶链反应、原位杂交和免疫组织化学评估肠系膜脂肪组织合成的PPARγ和炎性细胞因子。
在体内,克罗恩病患者存在腹腔内脂肪的重要堆积。这种从疾病发作起就存在的肠系膜肥胖与PPARγ及肿瘤坏死因子(TNF)-α的过表达相关,TNF-α至少部分由脂肪细胞合成。
这些结果表明,局限于肠系膜的PPARγ浓度升高可能导致肠系膜脂肪肥大,而肠系膜脂肪肥大可能通过合成TNF-α积极参与炎症反应。