ArticleCellular and molecular gastroenterology and hepatology2017
Intestinal Epithelial-Specific mTORC1 Activation Enhances Intestinal Adaptation After Small Bowel Resection.
Article in Cellular and molecular gastroenterology and hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Biological Insights into Intestinal Adaptation from Preclinical Models of Short Bowel Syndrome.Cells · 2026Review
- TNFR1 signaling connects inflammation to impaired fatty acid oxidation to drive intestinal stem cell aging.Nature aging · 2026Article
- Cellular senescence in human liver under normal aging and cancer.Cell genomics · 2026Article
- Enteroendocrine cell differentiation: Implications for human disease.Molecular and cellular endocrinology · 2025Review
- Metabolic regulation of intestinal homeostasis: molecular and cellular mechanisms and diseases.MedComm · 2024Review
- Analyzing efficiency of a lentiviral shRNA knockdown system in human enteroids using western blot and flow cytometry.STAR protocols · 2024Article
- Review
- Amino acid transporter SLC7A5 regulates cell proliferation and secretary cell differentiation and distribution in the mouse intestine.International journal of biological sciences · 2024Article
- Maternal docosahexaenoic acid supplementation during lactation improves exercise performance, enhances intestinal glucose absorption and modulates gut microbiota in weaning offspring mice.Frontiers in nutrition · 2024Article
- Increased epithelial mTORC1 activity in chronic rhinosinusitis with nasal polyps.bioRxiv : the preprint server for biology · 2023Article
- Okadaic Acid Is at Least as Toxic as Dinophysistoxin-1 after Repeated Administration to Mice by Gavage.Toxins · 2023Article
- A New Role for Endocrine Cells in the Intestinal Crypt.Cellular and molecular gastroenterology and hepatology · 2023Article
- mTOR as a Potential Target for the Treatment of Microbial Infections, Inflammatory Bowel Diseases, and Colorectal Cancer.International journal of molecular sciences · 2022Review
- A novel maladaptive unfolded protein response as a mechanism for small bowel resection-induced liver injury.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- How autophagy controls the intestinal epithelial barrier.Autophagy · 2022Review
- Article
- Acceleration of Small Intestine Development and Remodeling of the Microbiome Following Hyaluronan 35 kDa Treatment in Neonatal Mice.Nutrients · 2021Article
- Adaptation of extracellular matrix to massive small bowel resection in mice.Journal of pediatric surgery · 2020Article
- Gut epithelial TSC1/mTOR controls RIPK3-dependent necroptosis in intestinal inflammation and cancer.The Journal of clinical investigation · 2020Article
- Insulin-like Growth Factor-1 and mTORC1 Signaling Promote the Intestinal Regenerative Response After Irradiation Injury.Cellular and molecular gastroenterology and hepatology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsIntestinal adaptation is a compensatory response to the massive loss of small intestine after surgical resection. We investigated the role of intestinal epithelial cell-specific mammalian target of rapamycin complex 1 (i-mTORC1) in intestinal adaptation after massive small bowel resection (SBR).
methodsWe performed 50% proximal SBR on mice to study adaptation. To manipulate i-mTORC1 activity,
resultsAfter SBR, mice treated with systemic rapamycin showed diminished structural adaptation, blunted crypt cell proliferation, and significant body weight loss. Activating i-mTORC1 via TSC1 deletion induced larger hyperproliferative crypts and disorganized Paneth cells without a significant change in villus height. After SBR, ablating TSC1 in intestinal epithelium induced a robust villus growth with much stronger crypt cell proliferation, but similar body weight recovery. Acute inactivation of i-mTORC1 through deletion of Raptor did not change crypt cell proliferation or mucosa structure, but significantly reduced lysozyme/matrix metalloproteinase-7-positive Paneth cell and goblet cell numbers, with increased enteroendocrine cells. Surprisingly, ablation of intestinal epithelial cell-specific Raptor after SBR did not affect adaptation or crypt proliferation, but dramatically reduced body weight recovery after surgery.
conclusionsSystemic, but not intestinal-specific, mTORC1 is important for normal adaptation responses to SBR. Although not required, forced enterocyte mTORC1 signaling after resection causes an enhanced adaptive response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.