Role of Adipose Tissue in Inflammatory Bowel Disease

Abstract

Inflammatory bowel diseases (IBDs), chronic inflammatory disorders affecting the gastrointestinal tract, include Crohn's disease and ulcerative colitis. There are increasing clinical and experimental data showing that obesity, especially visceral adiposity, plays a substantial role in the pathogenesis of IBD. Obesity seems to be an important risk factor also for IBD disease severity and clinical outcomes. Visceral adipose tissue is an active multifunctional metabolic organ involved in lipid storage and immunological and endocrine activity. Bowel inflammation penetrates the surrounding adipose tissue along the mesentery. Mesenteric fat serves as a barrier to inflammation and controls immune responses to the translocation of gut bacteria. At the same time, mesenteric adipose tissue may be the principal source of cytokines and adipokines responsible for inflammatory processes associated with IBD. This review is particularly focusing on the potential role of adipokines in IBD pathogenesis and their possible use as promising therapeutic targets.

Keywords: adipokines; inflammatory bowel disease; mesenteric fat; microbiome; visceral obesity.

Figure 1

Distribution of abdominal adipose tissue in healthy state and visceral obesity. Adapted from Eder et al. [27].

Figure 2

Differences between mesenteric adipose tissue in healthy individuals and patients with IBD. Adapted from [3]. In contrast to lean state, creeping fat is characterized by smaller, highly active adipocytes, with enhanced expression of pro-inflammatory mediators (TNF-α, IL-6, etc.). Mesenteric adipose tissue is infiltrated by immune cells (macrophages, lymphocytes) with enhanced production of chemokines (MCP-1, M-CSF). In addition, pre-adipocytes can differentiate into macrophages. TNF-α, Tumor necrosis factor α; IL, Interleukin; MCP-1, Monocyte chemotactic protein-1; M-CSF, Macrophage colony-stimulating factor.