Inflammatory bowel diseases (IBDs) are a heterogeneous group of disorders exhibited by two major phenotypic forms:
Crohn's disease and
ulcerative colitis. Although the aetiology of IBD is unknown, several factors coming from the adipose tissue and skeletal muscles, such as
cytokines,
adipokines and
myokines, were suggested in the pathogenesis of
ulcerative colitis; however, it has not been extensively studied whether voluntary exercise can ameliorate that disorder. We explored the effect of moderate exercise (i.e., voluntary wheel running) on the disease activity index (DAI), colonic blood flow (CBF), plasma irisin and
adiponectin levels and real-time PCR expression of proinflammatory markers in mesenteric fat in mice with 2,4,6-trinitrobenzenesulfonic
acid (TNBS)
colitis fed a high-fat diet (HFD) compared to those on a standard chow diet (SD). Macroscopic and
microscopic colitis in sedentary SD mice was accompanied by a significant fall in CBF, some increase in colonic tissue weight and a significant increase in the plasma levels of tumour
necrosis factor-alpha (TNF-α),
IL-6,
monocyte chemotactic protein 1 (MCP-1) and
IL-13 (p < 0.05). In sedentary HFD mice, colonic lesions were aggravated, colonic tissue weight increased and the plasma TNF-α,
IL-6, MCP-1, IL-1β and
leptin levels significantly increased. Simultaneously, a significant decrease in the plasma irisin and
adiponectin levels was observed in comparison with SD mice (p < 0.05). Exercise significantly decreased macroscopic and
microscopic colitis, substantially increased CBF and attenuated the plasma TNF-α,
IL-6, MCP-1, IL-1β and
leptin levels while raising the plasma irisin and the plasma and WAT concentrations of
adiponectin in HFD mice (p < 0.05). We conclude that: (1) experimental
colitis is exacerbated in HFD mice, possibly due to a fall in colonic microcirculation and an increase in the plasma and mesenteric fat content of proinflammatory
biomarkers; and (2) voluntary physical activity can attenuate the severity of colonic damage in mice fed a HFD through the release of protective irisin and restoration of plasma
adiponectin.