Mechanisms of intestinal adaptation

Rubin, Deborah C.; Levin, Marc S.

doi:10.1016/j.bpg.2016.03.007

Cited by 52 publications

(41 citation statements)

References 84 publications

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“…14,37,38 Villous atrophy might be caused by either an increased rate of cell loss or a reduced rate of cell renewal, and increased crypt cell proliferation results in increased villus height, crypt depth and villus hyperplasia. 39 Furthermore, the proliferation (PCNA) and apoptosis (TUNEL) of epithelium was observed. The number of PCNA positive cells in both SD and CH mice was significantly decreased compared to control animals, and that of CH+SD animals was significantly decreased compared to SD animals.…”

Section: Discussionmentioning

confidence: 98%

The injury of serotonin on intestinal epithelium cell renewal of weaned diarrhoea mice

et al. 2016

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Diarrhoea is a common cause of death in children and weaned animals. Recent research has found that serotonin (5-HT) in the gastrointestinal tract plays an important role in regulating growth and the maintenance of mucosa, which protect against diarrhoea. To determine the influence of 5-HT on intestinal epithelium cell renewal under weaned stress diarrhoea, a weaned-stress diarrhoea mouse model was established with senna infusion (15 mL/Kg) via intragastric administration and stress restraint (SR). Mice with an increase in 5-HT were induced by intraperitoneal injection with citalopram hydrobromide (CH, 10 mg/Kg). The results demonstrated that compared with the control animals, diarrhoea appeared in weaned stress mice and the 5-HT content in the small intestine was significantly increased (P<0.05). Further, the caspase-3 cells and cells undergoing apoptosis in the small intestine were significantly increased, but the VH (villus height), V/C (villus height /crypt depth), and PCNA-positive rate significantly decreased. Compared with the control animals, CH increased the intestinal 5-HT content, caspase-3 cells and cells undergoing apoptosis but decreased the VH and V/C. Compared with both control and weaned stress animals, weaned stress animals that were pre-treated with CH showed higher 5-HT concentrations, positive caspase-3 cells and cells undergoing apoptosis but lower VH, V/C and PCNA-positive rate. In vitro, a low concentration of 5-HT inhibit, IEC-6 cell line apoptosis but a higher concentration of 5-HT promoted it. Therefore, weaned stress diarrhoea mice were accompanied by a 5-HT increase in the small intestine and vice versa, and the increase in 5-HT induced by CH caused diarrhoea. In brief, 5-HT and diarrhoea slowed the intestinal epithelium cell renewal and injured the abortion function and mucosal barrier by decreasing VH, V/C and proliferation and increasing epithelium cell apoptosis.

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Section: Discussionmentioning

confidence: 98%

The injury of serotonin on intestinal epithelium cell renewal of weaned diarrhoea mice

et al. 2016

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“…Resection of the stomach antrum decreases gastric acid secretion 103,104 and loss of absorptive surface in the duodenum and proximal jejunum reduces access to nutrient transporters 105 . At the same time, the adaptive response to changes in the anatomy result in growth of the remaining small intestine, similar to the adaptation of the gut that occurs after resection of the intestine, referred to as short gut syndrome 106 . The result of these changes is an increase the absorption of some nutrients but not others after RYGB 107 .…”

Section: Introductionmentioning

confidence: 98%

“…As aforementioned changes in gut anatomy, accompanied by intestinal hyperplasia 106,108 lead to changes in macronutrient absorption. Over the long term, the gut retains or enhances its ability to absorb glucose 109 , fatty acids 110 and amino acids 111,112 .…”

Section: Introductionmentioning

confidence: 99%

Proceedings of the 2017 ASPEN Research Workshop—Gastric Bypass: Role of the Gut

Jain

Roux

Puri

et al. 2018

J Parenter Enteral Nutr

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The goal of the National Institutes of Health-funded American Society for Parenteral and Enteral Nutrition 2017 research workshop (RW) "Gastric Bypass: Role of the Gut" was to focus on the exciting research evaluating gut-derived signals in modulating outcomes after bariatric surgery. Although gastric bypass surgery has undoubted positive effects, the mechanistic basis of improved outcomes cannot be solely explained by caloric restriction. Emerging data suggest that bile acid metabolic pathways, luminal contents, energy balance, gut mucosal integrity, as well as the gut microbiota are significantly modulated after bariatric surgery and may be responsible for the variable outcomes, each of which was rigorously evaluated. The RW served as a timely and novel academic meeting that brought together clinicians and researchers across the scientific spectrum, fostering a unique venue for interdisciplinary collaboration among investigators. It promoted engaging discussion and evolution of new research hypotheses and ideas, driving the development of novel ameliorative, therapeutic, and nonsurgical interventions targeting obesity and its comorbidities. Importantly, a critical evaluation of the current knowledge regarding gut-modulated signaling after bariatric surgery, potential pitfalls, and lacunae were thoroughly addressed.

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“…Short gut syndrome is a morbid clinical condition that follows a massive small bowel resection (SBR) required to treat several pediatric conditions such as necrotizing enterocolitis, midgut volvulus, and intestinal atresias (1) Intestinal adaptation is the response to massive SBR and is characterized by structural increases in crypt depth and villus height resulting in increased absorptive and digestive mucosal surface area (2, 3). The exact mechanisms for adaptation are incompletely understood and continues to be an area of research with the intent to achieve enteral autonomy in short gut patients.…”

Section: Introductionmentioning

confidence: 99%

Epithelial IGF1R is dispensable for IGF2 mediated enhanced intestinal adaptation in retinoblastoma-deficient mice

Sun

Choi

Diaz-Miron

et al. 2017

Journal of Pediatric Surgery

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Purpose Previously, we demonstrated enhanced adaptation after small bowel resection (SBR) in intestinal-specific Retinoblastoma (Rb) deficient mice along with elevated levels of insulin-like growth factor 2 (IGF2) expression within the villi. The purpose of this study was to verify that the insulin-like growth factor 1 receptor (IGF1R) plays a role in this phenomenon. Methods Inducible and intestinal specific Rb and IGF1R double knockout mice (iRb/IGF1R-IKO) (n=4) and Rb single knockout mice (iRb-IKO) (n=5) underwent 50% mid SBR. On post-operative day 28, mice were harvested, and structural adaptation was measured as changes in crypt depth and villus height. Rates of enterocyte proliferation were recorded. IGF2 expression within the remnant villi was measured via RT-PCR. Results Both iRb-IKO and iRb/IGF1R-IKO mice demonstrated enhanced adaptation with at least a 45% increase in both crypt depth and villus height in the proximal and distal remnant bowel. Both groups showed elevation of IGF2 expression in the remnant villi, but there were no differences between the two groups. Conclusion Epithelial IGF1R is dispensable for IGF2-mediated enhanced intestinal adaptation in retinoblastoma deficient mice. Our findings suggest that IGF2 signals for enhanced adaptation in cells outside of the epithelium. Further investigation is needed to study the IGF2/IGF1R signaling interaction within the mesenchyme.

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Mechanisms of intestinal adaptation

Cited by 52 publications

References 84 publications

The injury of serotonin on intestinal epithelium cell renewal of weaned diarrhoea mice

The injury of serotonin on intestinal epithelium cell renewal of weaned diarrhoea mice

Proceedings of the 2017 ASPEN Research Workshop—Gastric Bypass: Role of the Gut

Epithelial IGF1R is dispensable for IGF2 mediated enhanced intestinal adaptation in retinoblastoma-deficient mice

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