Objective: Obesity has gained attention among patients with inflammatory bowel disease (IBD). The impact of visceral obesity on chronic constipation, inflammation, immune function and cognition after diagnosis of IBD is still unknown. Methods: This is a cross-sectional study of 150 IBD patients. Patients’ visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were measured and were grouped according to visceral obesity. The potential impact of visceral obesity on cognitive function were evaluated using Mini-Mental State Examination. We evaluated patients’ incidence of chronic constipation, levels of interleukin-6 (IL-6), T cells and body mass index in two groups. Results: The prevalence of visceral obesity was 51% (37 out of 72) for Crohn’s disease (CD) patients and 26% for UC patients (20 out of 78 patients). CD patients with visceral obesity has higher incidence of chronic constipation (81% vs. 57%, P = 0.028), higher IL-6 levels (15.28 pg/ml vs. 9.429 pg/ml, P = 0.007) and lower CD4 + T cells (32.7% vs. 44.0%, P < 0.001). VAT/SAT ratio is associated with BMI ( P < 0.001). Conclusions: IBD patients had high risks of visceral obesity. CD Patients with visceral obesity had higher prevalence of chronic constipation, higher inflammation levels, decreased immune function.

Phosphorylation of signal transducer and activator of transcription 6 (STAT6) in the colonic epithelium is elevated in ulcerative colitis (UC) patients, and its inhibition prevents IL-13-associated apoptosis and barrier disruption. Recently, the STAT6 rs324015 polymorphism was reported to be related to genetic susceptibility to UC. Methods: We examined STAT6 rs324015 using the PCR-RFLP method in 268 UC cases and 357 controls. STAT6 expression was determined by quantitative reverse-transcription PCR. The gene-environment interactions were addressed by cross-over analysis. Results: We found that the STAT6 rs324015 polymorphism enhanced the risk of UC under the homozygous, dominant, and allelic models. Further subgroup analyses indicated that this relationship was more evident in alcohol users, smokers, and those younger than 40 years. Cross-over analysis showed strong interactions of STAT6 rs324015 with smoking/alcohol use. In addition, this polymorphism was associated with the severity, and location of UC. The GG genotype was significantly associated with increased STAT6 gene levels. Conclusion:In summary, the STAT6 rs324015 polymorphism is related with predisposition to UC in a Chinese Han population.

Objective: Obesity has gained attention among patients with inflammatory bowel disease (IBD). The impact of visceral obesity on chronic constipation, inflammation, immune function and cognition after diagnosis of IBD is still unknown.Methods: This is a cross-sectional study of 140 IBD patients. Patients’ visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were measured by abdominal computerized tomography (CT) scans and were grouped according to visceral obesity. Baseline variables, chronic constipation status, inflammation status and immune function were compared. The implications of visceral obesity on cognitive function were evaluated using Mini-Mental State Examination (MMSE).Results: The prevalence of visceral obesity was 51% (37 out of 72) for CD patients and 26% for UC patients (18 out of 68 patients). CD patients with visceral obesity has higher incidence of chronic constipation (81% vs. 57%, P = 0.028), higher IL-6 levels (15.28 pg/ml vs. 9.429 pg/ml, P = 0.0073) and lower CD4+ T cells (32.7% vs. 44.0%, P < 0.001). For UC patients, patients with visceral obesity have the tendency of higher IL-6 levels (7.2 vs. 6.0 pg/ml, P = 0.053). VAT/SAT ratio is associated with BMI (r = 0.652, P < 0.001).Conclusions: IBD patients had high risks of visceral obesity. CD Patients with visceral obesity had higher prevalence of chronic constipation, higher inflammation levels, decreased immune function.

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Background: Obesity has gained attention among patients with inflammatory bowel disease (IBD). The impact of visceral obesity on chronic obstipation, inflammation, immune function and cognition after diagnosis of IBD is still unknown.Methods: This is a cross-sectional study of 140 IBD patients. Patients’ visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were measured by abdominal computerized tomography (CT) scans and were grouped according to visceral obesity. Baseline variables, chronic obstipation status, inflammation status and immune function were compared. The implications of visceral obesity on cognitive function were evaluated using Mini-Mental State Examination (MMSE).Results: The prevalence of visceral obesity was 51% (37 out of 72) for CD patients and 26% for UC patients (18 out of 68 patients). CD patients with visceral obesity has higher incidence of chronic obstipation (81% vs. 57%, P = 0.028), higher IL-6 levels (9.3 vs. 6.0 pg/ml, P = 0.045) and lower CD4+ T cells (32.7% vs. 44.0%, P = 0.034). For UC patients, patients with visceral obesity have the tendency of higher IL-6 levels (7.2 vs. 6.0 pg/ml, P = 0.053).Conclusion: IBD patients had high risks of visceral obesity. Patients with visceral obesity had higher prevalence of chronic obstipation, higher inflammation levels, decreased immune function.

Background MicroRNAs are a class of small non-coding RNAs which act as oncogenes or tumor suppressors through targeting specific mRNAs. MiR-3622a-3p is found to be decreased in colorectal cancer (CRC) in TCGA database and there are few reports about the role of miR-3622a-3p in cancers. Our research aimed to explore the effect of miR-3622a-3p in CRC. Methods MiR-3622a-3p expression in CRC tissues and cells was examined by qRT-PCR. The effect of miR-3622a-3p on proliferation, apoptosis, cell cycle, migration and invasion of CRC cells were investigated by a serious of biological function assays. We performed dual luciferase assay to confirm the interaction between miR-3622a-3p and its potential target gene. Western blot was carried out to determine the effect of miR-3622a-3p on stemness features and EMT. Tumor xenograft model and in vivo metastasis model were established using nude mice. The CRC organoid model was constructed with fresh CRC tissues. Results MiR-3622a-3p was down-regulated in CRC tissues and cells. Biological function assays revealed that miR-3622a-3p could inhibit the malignant biological properties of CRC. MiR-3622a-3p suppressed stemness features and EMT of CRC cells by SALL4 mRNA degradation. The results of animal experiments showed miR-3622a-3p could inhibit CRC cell proliferation and metastasis in vivo . The growth of organoids was also suppressed by miR-3622a-3p. Conclusions Taken together, the results of our study indicate miR-3622a-3p exerts antioncogenic role in CRC by downregulation of SALL4. The research on miR-3622a-3p might provide a new insight into treatment of CRC.