Peptide YY and neuropeptide Y have potent antisecretory effects in rat small intestine. Scatchard analysis of [125I]peptide YY binding revealed a 10-fold higher concentration of receptors in rat jejunal crypt cells than in villus cells and no detectable receptors in colonic epithelium. Reverse transcription polymerase chain reaction analysis of neuropeptide Y Y5 receptor mRNA indicated that they are mainly expressed in rat jejunal crypts with very few or no expression in villus cells and colon epithelium, respectively. In order to determine whether neuropeptide Y Y5 receptors could represent the intestinal crypt receptor for peptide YY and neuropeptide Y, the ability of peptide YY, neuropeptide Y, pancreatic polypeptide and analogues to inhibit [125I]peptide YY binding to membrane prepared from rat crypt cells and COS-7 cells (African green monkey kidney cells) transfected with the rat neuropeptide Y Y5 receptor cDNA was tested. It appeared that several analogues displayed different inhibition constants (Ki) in the two binding assays, more especially N-alpha-acetyl-peptide YY-(22-36) which was 1200 x more potent in the crypt cell binding assay than in the recombinant neuropeptide Y Y5 receptor binding assay. These data support that the intestinal crypt peptide YY receptor is not a Y5 receptor. reserved.
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http://dx.doi.org/10.1016/s0014-2999(98)00757-2 | DOI Listing |
Front Nutr
January 2025
College of Animal Science, Anhui Science and Technology University, Chuzhou, China.
Introduction: Enterotoxic (ETEC) is the main pathogen that causes diarrhea, especially in young children. This disease can lead to substantial morbidity and mortality and is a major global health concern. Managing ETEC infections is challenging owing to the increasing prevalence of antibiotic resistance.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Cardiovascular, Endocrine-Metabolic Diseases and Aging, Istituto Superiore di Sanità, Rome, Italy.
Background: Bacterial toxins are emerging as promising hallmarks of colorectal cancer (CRC) pathogenesis. In particular, Cytotoxic Necrotizing Factor 1 (CNF1) from E. coli deserves special consideration due to the significantly higher prevalence of this toxin gene in CRC patients with respect to healthy subjects, and to the numerous tumor-promoting effects that have been ascribed to the toxin in vitro.
View Article and Find Full Text PDFUnited European Gastroenterol J
January 2025
Department of Gastroenterology, CHU Liège, Liège, Belgium.
Background And Aims: Probe-based confocal endomicroscopy (pCLE) allows real-time microscopic visualization of the intestinal mucosa surface layers. Despite remission achieved through anti-tumor necrosis factor or vedolizumab therapy, anomalies in the intestinal epithelial barrier are observed in inflammatory bowel disease (IBD) patients. Our study aimed to assess these abnormalities in non-IBD individuals and compare them with IBD patients in endoscopic remission to identify the associated factors.
View Article and Find Full Text PDFLife Med
October 2024
School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China.
Colorectal cancer (CRC), one of the most common tumors in the world, is generally proposed to be generated from intestinal stem cells (ISCs). Leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5)-positive ISCs are located at the bottom of the crypt and harbor self-renewal and differentiation capacities, serving as the resource of all intestinal epithelial cells and CRC cells as well. Here we review recent progress in ISCs both in non-tumoral and tumoral contexts.
View Article and Find Full Text PDFJ Anim Physiol Anim Nutr (Berl)
January 2025
Department Animal Science, Higher Education Complex of Torbat-e Jam, Torbat-e Jam, Iran.
This study aimed to compare the effects of dietary supplementation of bacteriophage (BP) and acidifiers on performance, meat quality, morphology, and intestinal microbiota in chickens challenged and unchallenged with Salmonella enteritidis (SE) and also to investigate the possibility of replacing them in the diet with antibiotics. A total of 1760 male Ross (308) chicks were randomly assigned to 11 dietary treatments (8 pens/with 20 male chickens in each). Dietary treatments were as follows: SE-uninfected (negative control (NC), a basal diet without supplemention; NC+ 500 g/t BP (NBP1); NC+ 1000 g/t BP (NBP2); NC+ 300 mg/kg acidifier A (NAA); NC+ 300 mg/kg acidifier B (NAB)) and SE-infected (positive control (PC), a basal diet without supplemention; PC+ 40 mg/kg Antibiotic enrofloxacin (PA); PC+ 500 g/t BP (PBP1); PC+ 1000 g/t BP (PBP2); PC+ 3000 mg/kg acidifier A (PAA); PC+ 3000 mg/kg acidifier B (PAB)).
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