71-OR: Oligofructose Improves Small Intestinal Nutrient-Sensing Mechanisms via the Small Intestinal Microbiota

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 71-OR
Author(s):  
SAVANNA N. WENINGER ◽  
EVE BEAUCHEMIN ◽  
ADELINA I.L. LANE ◽  
RACHEL MEYER ◽  
FRANK DUCA
Keyword(s):  
Intestinal Microbiota ◽  
Nutrient Sensing ◽  
Small Intestinal

scholarly journals Nutrient sensing by absorptive and secretory progenies of small intestinal stem cells

2017 ◽  
Vol 31 (S1) ◽  
Author(s):  
Kunihiro Kishida ◽  
Sarah Pearce ◽  
Shiyan Yu ◽  
Nan Gao ◽  
Ronaldo Ferraris
Keyword(s):  
Stem Cells ◽  
Nutrient Sensing ◽  
Intestinal Stem Cells ◽  
Small Intestinal

Rebamipide inhibits indomethacin-induced small intestinal injury: Possible involvement of intestinal microbiota modulation by upregulation of α-defensin 5

2013 ◽  
Vol 704 (1-3) ◽  
pp. 64-69 ◽  
Author(s):  
Tetsuya Tanigawa ◽  
Toshio Watanabe ◽  
Koji Otani ◽  
Yuji Nadatani ◽  
Fumikazu Ohkawa ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Intestinal Injury ◽  
Small Intestinal Injury ◽  
Small Intestinal

scholarly journals Nutrient sensing by absorptive and secretory progenies of small intestinal stem cells

2017 ◽  
Vol 312 (6) ◽  
pp. G592-G605 ◽  
Author(s):  
Kunihiro Kishida ◽  
Sarah C. Pearce ◽  
Shiyan Yu ◽  
Nan Gao ◽  
Ronaldo P. Ferraris
Keyword(s):  
Stem Cells ◽  
Cell Types ◽  
Paneth Cells ◽  
Nutrient Sensing ◽  
Intestinal Stem Cells ◽  
Intestinal Cell ◽  
Cell Type ◽  
Extended Lifespan ◽  
Small Intestinal ◽  
Single Cell Type

Nutrient sensing triggers responses by the gut-brain axis modulating hormone release, feeding behavior and metabolism that become dysregulated in metabolic syndrome and some cancers. Except for absorptive enterocytes and secretory enteroendocrine cells, the ability of many intestinal cell types to sense nutrients is still unknown; hence we hypothesized that progenitor stem cells (intestinal stem cells, ISC) possess nutrient sensing ability inherited by progenies during differentiation. We directed via modulators of Wnt and Notch signaling differentiation of precursor mouse intestinal crypts into specialized organoids each containing ISC, enterocyte, goblet, or Paneth cells at relative proportions much higher than in situ as determined by mRNA expression and immunocytochemistry of cell type biomarkers. We identified nutrient sensing cell type(s) by increased expression of fructolytic genes in response to a fructose challenge. Organoids comprised primarily of enterocytes, Paneth, or goblet, but not ISC, cells responded specifically to fructose without affecting nonfructolytic genes. Sensing was independent of Wnt and Notch modulators and of glucose concentrations in the medium but required fructose absorption and metabolism. More mature enterocyte- and goblet-enriched organoids exhibited stronger fructose responses. Remarkably, enterocyte organoids, upon forced dedifferentiation to reacquire ISC characteristics, exhibited a markedly extended lifespan and retained fructose sensing ability, mimicking responses of some dedifferentiated cancer cells. Using an innovative approach, we discovered that nutrient sensing is likely repressed in progenitor ISCs then irreversibly derepressed during specification into sensing-competent absorptive or secretory lineages, the surprising capacity of Paneth and goblet cells to detect fructose, and the important role of differentiation in modulating nutrient sensing. NEW & NOTEWORTHY Small intestinal stem cells differentiate into several cell types transiently populating the villi. We used specialized organoid cultures each comprised of a single cell type to demonstrate that 1) differentiation seems required for nutrient sensing, 2) secretory goblet and Paneth cells along with enterocytes sense fructose, suggesting that sensing is acquired after differentiation is triggered but before divergence between absorptive and secretory lineages, and 3) forcibly dedifferentiated enterocytes exhibit fructose sensing and lifespan extension.

scholarly journals Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB

2017 ◽  
Vol 97 (1) ◽  
pp. 411-463 ◽  
Author(s):  
Robert E. Steinert ◽  
Christine Feinle-Bisset ◽  
Lori Asarian ◽  
Michael Horowitz ◽  
Christoph Beglinger ◽  
...  
Keyword(s):  
Nutrient Sensing ◽  
Physiological Status ◽  
Healthy Weight ◽  
Endocrine Control ◽  
Synergistic Interactions ◽  
Local Signaling ◽  
Glucagon Like Peptide ◽  
Small Intestinal ◽  
Glucagon Like Peptide 1

The efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3–36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3–36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3–36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.

scholarly journals Rebamipide protects small intestinal mucosal injuries caused by indomethacin by modulating intestinal microbiota and the gene expression in intestinal mucosa in a rat model

2015 ◽  
Vol 56 (1) ◽  
pp. 20-27 ◽  
Author(s):  
Satoshi Kurata ◽  
Takako Nakashima ◽  
Takako Osaki ◽  
Naoya Uematsu ◽  
Masafumi Shibamori ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intestinal Microbiota ◽  
Intestinal Mucosa ◽  
Rat Model ◽  
Small Intestinal

scholarly journals The Nonsteroidal Anti-Inflammatory Drug Ketorolac Alters the Small Intestinal Microbiota and Bile Acids Without Inducing Intestinal Damage or Delaying Peristalsis in the Rat

2021 ◽  
Vol 12 ◽  
Author(s):  
Barbara Hutka ◽  
Bernadette Lázár ◽  
András S. Tóth ◽  
Bence Ágg ◽  
Szilvia B. László ◽  
...  
Keyword(s):  
Small Intestine ◽  
Bile Acids ◽  
Intestinal Microbiota ◽  
Intestinal Bacteria ◽  
Mucosal Inflammation ◽  
Intestinal Damage ◽  
Small Intestinal ◽  
Gi Transit ◽  
Anti Inflammatory ◽  
Conjugated Bile Acids

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) induce significant damage to the small intestine, which is accompanied by changes in intestinal bacteria (dysbiosis) and bile acids. However, it is still a question of debate whether besides mucosal inflammation also other factors, such as direct antibacterial effects or delayed peristalsis, contribute to NSAID-induced dysbiosis. Here we aimed to assess whether ketorolac, an NSAID lacking direct effects on gut bacteria, has any significant impact on intestinal microbiota and bile acids in the absence of mucosal inflammation. We also addressed the possibility that ketorolac-induced bacterial and bile acid alterations are due to a delay in gastrointestinal (GI) transit.Methods: Vehicle or ketorolac (1, 3 and 10 mg/kg) were given to rats by oral gavage once daily for four weeks, and the severity of mucosal inflammation was evaluated macroscopically, histologically, and by measuring the levels of inflammatory proteins and claudin-1 in the distal jejunal tissue. The luminal amount of bile acids was measured by liquid chromatography-tandem mass spectrometry, whereas the composition of microbiota by sequencing of bacterial 16S rRNA. GI transit was assessed by the charcoal meal method.Results: Ketorolac up to 3 mg/kg did not cause any signs of mucosal damage to the small intestine. However, 3 mg/kg of ketorolac induced dysbiosis, which was characterized by a loss of families belonging to Firmicutes (Paenibacillaceae, Clostridiales Family XIII, Christensenellaceae) and bloom of Enterobacteriaceae. Ketorolac also changed the composition of small intestinal bile by decreasing the concentration of conjugated bile acids and by increasing the amount of hyodeoxycholic acid (HDCA). The level of conjugated bile acids correlated negatively with the abundance of Erysipelotrichaceae, Ruminococcaceae, Clostridiaceae 1, Muribaculaceae, Bacteroidaceae, Burkholderiaceae and Bifidobacteriaceae. Ketorolac, under the present experimental conditions, did not change the GI transit.Conclusion: This is the first demonstration that low-dose ketorolac disturbed the delicate balance between small intestinal bacteria and bile acids, despite having no significant effect on intestinal mucosal integrity and peristalsis. Other, yet unidentified, factors may contribute to ketorolac-induced dysbiosis and bile dysmetabolism.

scholarly journals Effects of protease and phytase supplements on small intestinal microbiota and amino acid digestibility in broiler chickens

2019 ◽  
Vol 98 (7) ◽  
pp. 2906-2918 ◽  
Author(s):  
D. Borda-Molina ◽  
T. Zuber ◽  
W. Siegert ◽  
A. Camarinha-Silva ◽  
D. Feuerstein ◽  
...  
Keyword(s):  
Amino Acid ◽  
Intestinal Microbiota ◽  
Broiler Chickens ◽  
Small Intestinal

scholarly journals Small intestinal microbiota composition and the prognosis of infants with ileostomy resulting from distinct primary diseases

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Tian Qian ◽  
Haitao Zhu ◽  
Li Zhu ◽  
Chao Chen ◽  
Chun Shen ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Microbiota Composition ◽  
Small Intestinal
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