| http://purl.uniprot.org/citations/23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23884889 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.org/dc/terms/identifier | "doi:10.2337/db13-0035"xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Cheng H."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Ding Y."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Hu X."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Xiao Y."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Yang C."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Mao J."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/author | "Hou N."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/pages | "3736-3746"xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/title | "Overnutrition stimulates intestinal epithelium proliferation through beta-catenin signaling in obese mice."xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://purl.uniprot.org/core/volume | "62"xsd:string |
| http://purl.uniprot.org/citations/23884889 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23884889 |
| http://purl.uniprot.org/citations/23884889 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23884889 |
| http://purl.uniprot.org/uniprot/#_D0FZQ3-mappedCitation-23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23884889 |
| http://purl.uniprot.org/uniprot/#_D3Z7S6-mappedCitation-23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23884889 |
| http://purl.uniprot.org/uniprot/#_D3Z5Q1-mappedCitation-23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23884889 |
| http://purl.uniprot.org/uniprot/#_E9Q6A9-mappedCitation-23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23884889 |
| http://purl.uniprot.org/uniprot/#_A0A338P6P8-mappedCitation-23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23884889 |
| http://purl.uniprot.org/uniprot/#_F7CRC6-mappedCitation-23884889 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23884889 |