ArticleEBioMedicine2018
Activation of mTORC1 signaling in gastric X/A-like cells induces spontaneous pancreatic fibrosis and derangement of glucose metabolism by reducing ghrelin production.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Potentiality of ghrelin as antioxidant and protective agent.Redox report : communications in free radical research · 2021Pooled it
- Organ cross-talk: molecular mechanisms, biological functions, and therapeutic interventions for diseases.Signal transduction and targeted therapy · 2026Review
- Intact mTOR signaling in gastric X/A-like cells is required for bone homeostasis.Frontiers in endocrinology · 2026Article
- Enteroendocrine cell differentiation: Implications for human disease.Molecular and cellular endocrinology · 2025Review
- Intestinal Enteroendocrine Cells: Present and Future Druggable Targets.International journal of molecular sciences · 2023Review
- Lower ghrelin levels does not impact the metabolic benefit induced by Roux-en-Y gastric bypass.Frontiers in endocrinology · 2022Article
- Ghrelin Based Therapy of Metabolic Diseases.Current medicinal chemistry · 2021Review
- Adipocyte-Specific Inhibition ofFrontiers in endocrinology · 2021Article
- Stomach 'tastes' the food and adjusts its emptying: A neurophysiological hypothesis (Review).Experimental and therapeutic medicine · 2020Review
- mTOR Pathway is Involved in Energy Homeostasis Regulation as a Part of the Gut-Brain Axis.International journal of molecular sciences · 2020Review
- Ghrelin Fights Against Titanium Particle-Induced Inflammatory Osteolysis Through Activation of β-Catenin Signaling Pathway.Inflammation · 2019Article
- A Novel Stomach-Pancreas Connection: More than Physical.EBioMedicine · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPancreatic fibrosis is a pathophysiological process associated with excessive deposition of extracellular matrix in pancreas, leading to reduced insulin secretion and derangement of glucose metabolism. X/A-like cells, a group of unique endocrine cells in gastric oxyntic mucosa, produce and secret ghrelin to influence energy balance. Whether gastric X/A-like cells affect pancreatic fibrosis and subsequent glucose homeostasis remains unclear.
methodsWe established a Ghrl-cre transgene in which the cre enzyme is expressed in X/A-like cells under the control of ghrelin-promoter. TSC1
findingsActivation of mTORC1 signaling by deletion of TSC1 gene in gastric X/A-like cells induced spontaneous pancreatic fibrosis. This alteration was associated with reduced insulin expression and secretion, as well as impaired glucose metabolism. Activation of mTORC1 signaling in gastric X/A-like cells reduced gastric and circulating ghrelin levels. Exogenous ghrelin reversed pancreatic fibrosis and glucose intolerance induced by activation of mTORC1 signaling in these cells. Rapamycin, an inhibitor of mTOR, reversed the decrease of ghrelin levels and pancreatic fibrosis.
interpretationActivation of mTORC1 signaling in gastric X/A-like cells induces spontaneous pancreatic fibrosis and subsequently impairs glucose homeostasis via suppression of ghrelin.
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Registered trials
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