Copyright
©The Author(s) 2025.
World J Gastroenterol. Jan 7, 2025; 31(1): 102042
Published online Jan 7, 2025. doi: 10.3748/wjg.v31.i1.102042
Published online Jan 7, 2025. doi: 10.3748/wjg.v31.i1.102042
Mechanism | Description | Ref. |
Bacterial translocation | Migration of bacteria from the intestinal lumen to the mesenteric adipose tissue, stimulating local inflammation | Ha et al[22] |
Chronic inflammation | Continuous production of inflammatory cytokines (such as tumor necrosis factor-α, interleukin-6, and interleukin-1β) that affect the mesentery | Wu et al[14]; Foppa et al[24] |
Local adipokine production | Release of leptin and adiponectin from adipose tissue, which modulates the immune and inflammatory responses | Tsounis et al[19] |
Hypoxia and local fibrosis | The expansion of mesenteric fat can generate hypoxia, favoring fibrosis and aggravating the inflammatory condition | Wu et al[14]; Li et al[33] |
Alteration of gut microbiota | Changes in the composition of the intestinal microbiota that affect the metabolism and function of the adipose tissue | Gilliland et al[4]; Ha et al[22] |
Activation of macrophages and T cells | Infiltration of macrophages and T cells into adipose tissue, perpetuating inflammation and tissue remodeling | Karaskova et al[12]; Tsounis et al[19] |
- Citation: Quaglio AE, Magro DO, Imbrizi M, De Oliveira EC, Di Stasi LC, Sassaki LY. Creeping fat and gut microbiota in Crohn’s disease. World J Gastroenterol 2025; 31(1): 102042
- URL: https://www.wjgnet.com/1007-9327/full/v31/i1/102042.htm
- DOI: https://dx.doi.org/10.3748/wjg.v31.i1.102042