Refeeding starved rats with an elemental diet resulted in a marked increase in crypt cell production rate (CCPR) in the proximal small intestine but not in the distal regions of the gut. Little effect on CCPR was noted when inert bulk (kaolin) was added to the elemental diet. Addition of a poorly fermentable dietary fibre (purified wood cellulose) had little effect on intestinal epithelial cell proliferation except in the distal colon where it significantly increased CCPR. A more readily fermentable fibre (purified wheat bran) caused a large proliferative response in the proximal, mid, and distal colon and in the distal small intestine. A gel forming fibre only significantly stimulated proliferation in the distal colon; the rats in this group, however, did not eat all the food given. There was no significant correlation between CCPR and plasma gastrin concentrations, but plasma enteroglucagon concentrations were significantly correlated with CCPR in almost all the sites studied. Plasma PYY concentrations also showed some correlation with CCPR, especially in the colon. Thus while inert bulk cannot stimulate colonic epithelial cell proliferation fermentable fibre is capable of stimulating proliferation in the colon, and especially in the distal colon: it can also stimulate proliferation in the distal small intestine and it is likely that plasma enteroglucagon may have a role to play in this process.
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http://dx.doi.org/10.1136/gut.28.2.171 | DOI Listing |
J Med Screen
January 2025
Cancer Screening and Prevention Research Group (CSPRG), Department of Surgery and Cancer, Imperial College London, London, UK.
Objectives: Colonoscopy surveillance is often performed in post-polypectomy cohorts, likely altering colorectal cancer (CRC) outcomes, but this is often not addressed in CRC incidence analyses. We examined CRC incidence post-endoscopic screening, accounting for surveillance.
Methods: We examined UK Flexible Sigmoidoscopy Screening Trial participants who had no, low-risk, or high-risk (≥10 mm, ≥3 adenomas, adenomas with villous features/high-grade dysplasia) distal polyps at screening.
Int J Mol Sci
January 2025
Molecular Diagnostic and Clinical Research Unit, University Hospital of Southern Denmark, 6200 Aabenraa, Denmark.
Inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract. Current immune-modulating therapies are insufficient for 30-50% of patients or cause significant side effects, emphasizing the need for new treatments. Targeting the innate immune system and enhancing drug delivery to inflamed gut regions are promising strategies.
View Article and Find Full Text PDFDis Colon Rectum
February 2025
Department of Colorectal Surgery, Digestive Disease and Surgery Institute, Cleveland Clinic, Ohio.
Background: Patients with Crohn's disease face an elevated risk of colorectal cancer, in part due to underlying chronic inflammation. Biologic therapy is the mainstay of medical treatment; however, the impact of treatment on colorectal cancer-related outcomes remains unclear.
Objective: To investigate the association between prior exposure to biologic treatment and colorectal cancer-related outcomes in patients with underlying Crohn's disease.
Dis Colon Rectum
February 2025
Department of General Surgery, Jinling Medical School of Nanjing Medical University, Nanjing, China.
Background: Even in the biological era, permanent stoma is not uncommon in patients with Crohn's Disease.
Objective: This study aimed to investigate the incidence and risk factors of permanent stoma in Crohn's disease patients and provide clinical evidence for reducing this disabling outcome.
Design: Consecutive patients with Crohn's disease who underwent ostomies in the past decade were reviewed.
Int J Epidemiol
December 2024
International Agency for Research on Cancer (IARC/WHO), Nutrition and Metabolism Branch, Lyon, France.
Background: Adiposity is an established risk factor for colorectal cancer (CRC). The pathways underlying this relationship, and specifically the role of circulating proteins, are unclear.
Methods: Utilizing two-sample univariable Mendelian randomization (UVMR), multivariable Mendelian randomization (MVMR), and colocalization, based on summary data from large sex-combined and sex-specific genetic studies, we estimated the univariable associations between: (i) body mass index (BMI) and waist-hip ratio (WHR) and overall and site-specific (colon, proximal colon, distal colon, and rectal) CRC risk, (ii) BMI and WHR and circulating proteins, and (iii) adiposity-associated circulating proteins and CRC risk.
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