P-CAB improved the efficacy of CAM-containing 7-day triple therapy and would be a valuable first-line treatment for H. pylori infection.

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Mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) is an important target in the treatment of inflammatory bowel disease (IBD). Recently, treatment of IBD with an antibody to alpha4beta7-integrin, a ligand for MAdCAM-1, has been an intense focus of research. Our aim was to clarify the mechanism by which MAdCAM-1 is regulated via angiotensin II type 1 receptor (AT1R), and to verify if AT1R might be a novel target for IBD treatment. The role of AT1R in the expression of MAdCAM-1 in SVEC (a murine high endothelial venule cell) and MJC-1 (a mouse colonic endothelial cell) was examined following cytokine stimulation. We further evaluated the effect of AT1R on the pathogenesis of immune-mediated colitis using AT1R-deficient (AT1R-/-) mice and a selective AT1R blocker. AT1R blocker significantly suppressed MAdCAM-1 expression induced by TNF-alpha, but did not inhibit phosphorylation of p38 MAPK or of IkappaB that modulate MAdCAM-1 expression. However, NF-kappaB translocation into the nucleus was inhibited by these treatments. In a murine colitis model induced by dextran sulfate sodium, the degree of colitis, judged by body weight loss, histological damage, and the disease activity index, was much milder in AT1R-/- than in wild-type mice. The expression of MAdCAM-1 was also significantly lower in AT1R-/- than in wild-type mice. These results suggest that AT1R regulates the expression of MAdCAM-1 under colonic inflammatory conditions through regulation of the translocation of NF-kappaB into the nucleus. Furthermore, inhibition of AT1R ameliorates colitis in a mouse colitis model. Therefore, AT1R might be one of new therapeutic target of IBD via regulation of MAdCAM-1.

Background/Aims: Evidence suggests that intestinal microbiota, along with factors such as diet and host genetics, contributes to obesity, metabolic dysfunction and diabetes. Therefore, we examined the relationship between gut microbiota, blood metabolic markers, dietary habits and fecal short-chain fatty acids (SCFAs) in patients with type 2 diabetes mellitus (T2DM). Methods: Dietary habits, blood and fecal samples from 59 T2DM patients were recruited, and the association of intestinal microbiota with metabolic markers and dietary habits was analyzed. Results: Total energy intake was 1,692 ± 380 kcal/day. Carbohydrate, fat and protein intakes were 57.5 ± 5.2, 23.2 ± 5.3 and 13.2 ± 2.2%, respectively. Dietary habits - high carbohydrate, fat, and protein intake - were associated with increased counts of Clostridium clusters IV and XI and decreased counts of Bifidobacterium spp., order Lactobacillales and Clostridium cluster IV. Protein intake was negatively correlated with fecal acetate and total SCFAs. Total SCFAs, propionate and acetate were negatively correlated with blood insulin levels and the homeostasis model of insulin resistance. Conclusion: Diets low in protein and carbohydrates favor a healthy gut microbiome and improve glucose tolerance in T2DM patients, although further elucidation of the role of the gut microbiome could lead to better therapies and prophylaxes.

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