ArticleDiabetes2013
Overnutrition stimulates intestinal epithelium proliferation through β-catenin signaling in obese mice.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 121 citations in OpenAlex.
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- High-fat diet, intestinal microecology and bone loss.Nutrition & metabolism · 2025Review
- Human adaptation response to obesity.International journal of obesity (2005) · 2025Review
- Reduction of intestinal RIPK1 ameliorates HFD-induced metabolic disorders in female mice.iScience · 2025Article
- Dietary and metabolic effects on intestinal stem cells in health and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Effects of maternal overnutrition and metabolic challenge in adult life on the histological integrity of the liver and intestinal epithelium in rabbits.Frontiers in nutrition · 2025Article
- Breed-Driven Microbiome Heterogeneity Regulates Intestinal Stem Cell Proliferation via Lactobacillus-Lactate-GPR81 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Silicon as a Functional Meat Ingredient Improves Jejunal and Hepatic Cholesterol Homeostasis in a Late-Stage Type 2 Diabetes Mellitus Rat Model.Foods (Basel, Switzerland) · 2024Article
- Intestinal Microbiota Increases Cell Proliferation of Colonic Mucosa in Human-Flora-Associated (HFA) Mice.International journal of molecular sciences · 2024Article
- Multiomics analysis reveals that microbiota regulate fat and muscle synthesis in chickens.Poultry science · 2024Article
- Nutrigenomic underpinnings of intestinal stem cells in inflammatory bowel disease and colorectal cancer development.Frontiers in genetics · 2024Review
- Industrialized human gut microbiota increases CD8+ T cells and mucus thickness in humanized mouse gut.Gut microbes · 2023Article
- Perturbation of intestinal stem cell homeostasis and radiation enteritis recovery via dietary titanium dioxide nanoparticles.Cell proliferation · 2023Article
- Association of a high-fat diet with I-FABP as a biomarker of intestinal barrier dysfunction driven by metabolic changes in Wistar rats.Lipids in health and disease · 2023Article
- Obesity and cancer stem cells: Roles in cancer initiation, progression and therapy resistance.World journal of stem cells · 2023Review
- The intestinal permeability marker FITC-dextran 4kDa should be dosed according to lean body mass in obese mice.Nutrition & diabetes · 2023Article
- Obesity under the moonlight of c-MYC.Frontiers in cell and developmental biology · 2023Review
- Intestinal plasticity and metabolism as regulators of organismal energy homeostasis.Nature metabolism · 2022Review
- Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is a major risk factor for type 2 diabetes and cardiovascular diseases. And overnutrition is a leading cause of obesity. After most nutrients are ingested, they are absorbed in the small intestine. Signals from β-catenin are essential to maintain development of the small intestine and homeostasis. In this study, we used a hyperphagia db/db obese mouse model and a high-fat diet (HFD)-induced obesity mouse model to investigate the effects of overnutrition on intestinal function and β-catenin signaling. The β-catenin protein was upregulated along with inactivation of glycogen synthase kinase (GSK)-3β in the intestines of both db/db and HFD mice. Proliferation of intestinal epithelial stem cells, villi length, nutrient absorption, and body weight also increased in both models. These changes were reversed by caloric restriction in db/db mice and by β-catenin inhibitor JW55 (a small molecule that increases β-catenin degradation) in HFD mice. Parallel, in vitro experiments showed that β-catenin accumulation and cell proliferation stimulated by glucose were blocked by the β-catenin inhibitor FH535. And the GSK-3 inhibitor CHIR98014 in an intestinal epithelial cell line increased β-catenin accumulation and cyclin D1 expression. These results suggested that, besides contribution to intestinal development and homeostasis, GSK-3β/β-catenin signaling plays a central role in intestinal morphological and functional changes in response to overnutrition. Manipulating the GSK-3β/β-catenin signaling pathway in intestinal epithelium might become a therapeutic intervention for obesity induced by overnutrition.
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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.