Mesenteric adipose tissue: from protective gatekeeper to driver of inflammatory bowel disease

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Inflammatory bowel disease (IBD) defines a group of diseases, including Crohn's disease and ulcerative colitis, characterized by chronic inflammation of the gastrointestinal tract. Evidence suggests that visceral adipose tissue, particularly its mesenteric component, influences the course of IBD through its immunomodulatory properties. Mesenteric adipose tissue (MAT) is composed of multiple cell types, including adipocytes, preadipocytes, and immune cells, that collectively regulate energy balance and endocrine signaling. MAT is a unique fat depot as it directly connects along most of the intestinal serosa and harbors the arteries, veins, and lymph nodes that support intestinal function. MAT's placement at the intestinal barrier serves to contain microbial translocation and support the repair of intestinal epithelium. However, inflammation initiated by obesity or IBD renders it maladaptive, triggering an influx of immune cells that, in turn, release proinflammatory adipokines, cytokines, and chemokines, resulting in local and systemic metabolic effects. Clinical data strongly link the accumulation of inflammatory MAT in the pathology of Crohn's disease through the development of "creeping fat", a fibrotic, immune-rich tissue that shields the inflamed bowel but can also exacerbate the condition. The inflammatory mediators produced by MAT and the mechanisms by which they aggravat

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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