Abstract

Abstract Background Obesity, impaired glucose tolerance and unfavorable lipid profile are established risk factors for cardiovascular disease. Patients with inflammatory bowel disease (IBD) may be at increased risk of cardiovascular disease, and new therapies such as JAK inhibitors may further add to this risk. C-reactive protein (CRP) is a marker of systemic inflammation that may increase with active IBD and is correlated with metabolic risk in non-IBD cohorts. Diet, in particular consumption of ultra-processed foods, has been linked to gut dysbiosis and the onset, course, and response to treatment of both IBD and metabolic disease. The aim of this study was to identify metabolic risk in a cohort of individuals with IBD through an analysis of diet, metabolic parameters and stool microbial diversity. Methods This two-week prospective case-control study enrolled non-diabetic individuals with IBD in clinical remission and healthy individuals (HC). Baseline body mass index (BMI), waist circumference (WC) and waist to hip ratio, detailed diet diary, serum metabolic and inflammatory parameters, stool bacterial microbiota and faecal calprotectin (FC) were examined. Results Eighty-one participants; 57 with IBD (26 ulcerative colitis (UC), 31 Crohn’s disease (CD)) and 24 HC participants were recruited. In the IBD group, there was a positive correlation between serum insulin, triglycerides, BMI and WC with CRP and a negative correlation between HDL and CRP (Table 1). There were no associations between measured metabolic risk factors and FC. Stool microbial alpha diversity of the IBD group was lower than that of the HC cohort, with lower species richness (IBD 21.4 v HC 26.8, p<0.01) and Shannon’s diversity index (SDI) (IBD 3.1 v HC 3.4, p=0.03) (Figure 1). In the IBD group, there was a negative association between serum insulin and CRP with stool species evenness (SE) and SDI (insulin: SE r=-0.41, adj-p=0.02, SDI r=-0.39, adj-p=0.02; CRP: SE r=-0.4, p=0.02, SDI r=-0.4, p=0.02) and a negative association between intake of processed meat and stool alpha diversity metrics (SE r=-0.39, adj-p=0.046 and SDI r=-0.42, adj-p=0.02 respectively). There were no significant associations between serum metabolic profile and dietary intake with stool alpha diversity in the HC group. Conclusion Unhealthy diet, higher body weight and suboptimal glucose control were positively associated with CRP in participants with IBD. Gut microbiota with reduced diversity may be a common link between adverse metabolic outcomes and IBD. Serum insulin should be explored as a common biomarker of metabolic and gut microbial health.

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