Abstract
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.
Highlights
Inflammatory bowel diseases (IBDs) pertain to a group of disorders of inflammatory conditions of the colon and small intestine that display two major phenotypic forms: Crohn’s disease (CD)and ulcerative colitis (UC), both characterized by a cyclical nature alternating between active and quiescent states [1]
Diet-induced obesity (DIO) obtained by feeding rodents on high-fat diets is the most common model reported in the literature because DIO mimics the human characteristics of obesity and leads to increased mesenteric fat deposition, colonic inflammation and deterioration in experimental colitis [6,7,8,9]
A double cross indicates achange significant compared to the high-fat diet (HFD) mice without voluntary exercise (p < 0.05, ANOVA)
Summary
Inflammatory bowel diseases (IBDs) pertain to a group of disorders of inflammatory conditions of the colon and small intestine that display two major phenotypic forms: Crohn’s disease (CD)and ulcerative colitis (UC), both characterized by a cyclical nature alternating between active and quiescent states [1]. In CD, the hypertrophied mesenteric white adipose tissue (mWAT) could be a major contributor to the increase in the circulating proinflammatory cytokines and play a role in the pathogenesis and disease activity [2,3,4,5]. Diet-induced obesity (DIO) obtained by feeding rodents on high-fat diets is the most common model reported in the literature because DIO mimics the human characteristics of obesity and leads to increased mesenteric fat deposition, colonic inflammation and deterioration in experimental colitis [6,7,8,9]. Increased aerobic activity, designed for IBD patients, has been recommended for obtaining good overall health, reversing muscle weakness and improving bone mineral density [10]
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