Diabetes mellitus is a chronic disease requiring lifelong medical attention. With hundreds of millions suffering worldwide, and a rapidly rising incidence, diabetes mellitus poses a great burden on healthcare systems. Recent studies investigating the underlying mechanisms involved in disease development in diabetes point to the role of the dys-regulation of the intestinal barrier. Via alterations in the intestinal permeability, intestinal barrier function becomes compromised whereby access of infectious agents and dietary antigens to mucosal immune elements is facilitated, which may eventually lead to immune reactions with damage to pancreatic beta cells and can lead to increased cytokine production with consequent insulin resistance. Understanding the factors regulating the intestinal barrier function will provide important insight into the interactions between luminal antigens and immune response elements. This review analyses recent advances in the mechanistic understanding of the role of the intestinal epithelial barrier function in the development of type 1 and type 2 diabetes. Given our current knowledge, we may assume that reinforcing the intestinal barrier can offer and open new therapeutic horizons in the treatment of type 1 and type 2 diabetes.

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Summary Background  The gastrointestinal tract elicits numerous signals regulating food intake and satiety, and recently many studies have been performed to elucidate the mechanisms regulating these signals. Aim  To describe the effects of the gastrointestinal tract on satiety, satiation and food intake. Methods  A PubMed search was performed to identify and select the relevant literature using search terms including ‘gastric satiety, intestine + satiety, satiation, cholecystokinin, ghrelin, peptide YY, glucagon‐like peptide‐1 and ileal brake’. Results  Satiation, satiety and food intake result, among other factors, from signals originating in the stomach caused by distension and signals from the small intestine. These intestinal signals result from nutrient sensing in the gut and activate neural and humoral pathways. Activation of the distal part of the gut, the so called ileal brake, leads to reduction in hunger and food intake, and models of chronic ileal brake activation lead to massive weight loss. Conclusion  Gastrointestinal signals are crucial for the regulation of food intake, satiety and satiation. The ileal brake deserves special attention, as both ileal intubation studies and surgical studies demonstrate that activation of the ileal brake reduces food intake. In the surgical models, weight loss occurs without adaptation to the anorectic effects of ileal brake activation.

The aim of this review was to examine the nature of GI symptoms and their underlying pathophysiology in JHS/EDS-HT. In addition, we consider the clinical implications of the diagnosis and treatment of JHS/EDS-HT for practicing clinicians in gastroenterology. Observations summarized in this review may furthermore represent the first step toward the identification of a new pathophysiological basis for a substantial subgroup of patients with functional GI disorders.

Several studies have raised warnings about the limited effectiveness of colonoscopy for the prevention of colorectal cancer (CRC), especially of the proximal colon. Two major categories of factors might be responsible for the development of interval cancers, namely technical, endoscopist-dependent factors and biological characteristics of the cancer that lead to more rapid tumour progression. Recognition of endoscopist-dependent factors is critical, as these factors are probably amenable to correction through improved awareness and education of endoscopists, using quality metrics (such as adenoma detection rates and cecal intubation rates) for objective evaluation and feedback. In this article, the current literature regarding the incidence of, and potential explanations for, interval CRCs is outlined. Although there is probably an interaction between technical and biology-related factors--and an attempt to dissect the biology from the technology might be fraught with difficulties--a structured analysis of individual cases of interval cancer might help in the continuous monitoring of the quality of colonoscopy, and ultimately might reduce the number of interval CRCs.

Electronic nose (e-nose) technology has the potential to detect cancer at an early stage and can differentiate between cancer origins. Our objective was to compare patients who had head and neck squamous cell carcinoma (HNSCC) with patients who had colon or bladder cancer to determine the distinctive diagnostic characteristics of the e-nose. Feasibility study An e-nose device was used to collect samples of exhaled breath from patients who had HNSCC and those who had bladder or colon cancer, after which the samples were analyzed and compared. One hundred patients with HNSCC, 40 patients with bladder cancer, and 28 patients with colon cancer exhaled through an e-nose for 5 min. An artificial neural network was used for the analysis, and double cross-validation to validate the model. In differentiating HNSCC from colon cancer, a diagnostic accuracy of 81 % was found. When comparing HNSCC with bladder cancer, the diagnostic accuracy was 84 %. A diagnostic accuracy of 84 % was found between bladder cancer and colon cancer. The e-nose technique using double cross-validation is able to discriminate between HNSCC and colon cancer and between HNSCC and bladder cancer. Furthermore, the e-nose technique can distinguish colon cancer from bladder cancer.

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Background: Patient perception of colonoscopy varies greatly. Young slender women and patients with irritable bowel syndrome (IBS) appear to be at risk for periprocedural pain. Recent evidence suggests a high prevalence of joint hypermobility related connective tissue disorders in this population. Therefore, we aimed to investigate whether hypermobility spectrum disorder (HSD) is associated with increased pain during colonoscopy. Methods: We prospectively included patients undergoing routine colonoscopy. Subjects were assessed for HSD using the 2017 criteria, and IBS and functional dyspepsia using the Rome III criteria. After colonoscopy and recovery from sedation, patients were asked to report pain scores on a 100-mm visual analogue scale (VAS). In addition, caecal intubation time was measured, endoscopists scored the difficulty of the procedure (100-mm VAS) and procedure-related adverse events were registered. Results: Of 200 included patients, 22 (11%) met criteria for HSD. A female predominance was observed in patients with HSD (86.4% versus 49.4%, p < 0.001). A crude linear regression model demonstrated that pain scores were 13.30 mm higher in patients with HSD versus non-HSD patients (95% CI 0.07 – 26.53, p = 0.049). When subsequently correcting for possible confounding factors, however, this difference in pain scores could be explained by a confounding effect of female gender. Caecal intubation time, perceived procedural difficulty and complication rate did not differ significantly between groups. Conclusion: HSD does not seem to be a predictor of painful colonoscopy, probably due to female gender as a confounding factor. In addition, performing colonoscopy is not more complicated in patients with HSD versus non-HSD patients, nor is it associated with more adverse events.