Department of Medicine II (Gastroenterology and Hepatology), Medical University Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.
Curr Drug Deliv. 2012 Jul;9(4):326-32. doi: 10.2174/156720112801323044.
Mesenteric fat hypertrophy is a common feature of inflammatory bowel diseases (IBD), especially Crohn's disease. Although this "creeping fat" has been observed in the early days of this disease, its biological relevance is not understood. This adipose tissue has been recognized to release large amounts of various cytokines such as TNFa and adipocytokines such as adiponectin or leptin. Whereas leptin is definitely a pro-inflammatory adipocytokine, the role of the prototypic anti-inflammatory adipocytokine, namely adiponectin, in intestinal inflammation is less clear. Some experimental studies suggest that it could exert also pro-inflammatory activities in the gut. An important role for metabolic aspects and potentially adipocytokines has also come from recent studies demonstrating that ATG16L1- deficient mice show a strikingly enhanced expression of both adiponectin and leptin in epithelial cells. Autophagy not only plays a key role in intestinal inflammation, but is also involved in the regulation of lipid metabolism. Another recently identified pathway in IBD, namely endoplasmic stress/XBP1, regulates fatty acid synthesis and facilitates adipogenesis and adipocyte differentiataion. Therefore, XBP1 could possibly link intestinal inflammation with the development of "creeping fat" in Crohn's disease. Metabolic aspects have evolved as of key importance in experimental colitis and human IBD, and certain adipocytokines, autophagy, and ER stress might reflect the central players.
肠系膜脂肪肥大是炎症性肠病（IBD）的一个常见特征，尤其是克罗恩病。虽然这种“ creeping fat ”在这种疾病的早期就已经被观察到，但它的生物学相关性尚不清楚。这种脂肪组织已被证实会释放大量的各种细胞因子，如 TNFa 和脂肪细胞因子，如脂联素或瘦素。虽然瘦素绝对是一种促炎脂肪细胞因子，但原型抗炎脂肪细胞因子脂联素在肠道炎症中的作用尚不清楚。一些实验研究表明，它在肠道中也可能发挥促炎作用。代谢方面和潜在的脂肪细胞因子的重要作用也来自最近的研究，这些研究表明，ATG16L1 缺陷小鼠在肠上皮细胞中表现出脂联素和瘦素的表达显著增强。自噬不仅在肠道炎症中起着关键作用，而且还参与脂质代谢的调节。IBD 中另一个最近确定的途径，即内质网应激/XBP1，调节脂肪酸合成，并促进脂肪生成和脂肪细胞分化。因此，XBP1 可能将肠道炎症与克罗恩病中“ creeping fat ”的发展联系起来。代谢方面在实验性结肠炎和人类 IBD 中已经变得至关重要，某些脂肪细胞因子、自噬和 ER 应激可能反映了主要参与者。
