http://purl.uniprot.org/citations/22719219 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/22719219 | http://www.w3.org/2000/01/rdf-schema#comment | "ObjectiveThe WNT signaling pathway effector gene TCF7L2 has been associated with an increased risk of type 2 diabetes. However, it remains unclear how this gene affects diabetic pathogenesis. The goal of this study was to investigate the effects of Tcf7l2 haploinsufficiency on metabolic phenotypes in mice.Experimental designTcf7l2 knockout (Tcf7l⁻/⁻) mice were generated. Because of the early mortality of Tcf7l2⁻/⁻ mice, we characterized the metabolic phenotypes of heterozygous Tcf7l2⁺/⁻ mice in comparison to the wild-type controls. The mice were fed a normal chow diet or a high fat diet (HFD) for 9 weeks.ResultsThe Tcf7l2⁺/⁻ mice showed significant differences from the wild-type mice with regards to body weight, fasting glucose and insulin levels. Tcf7l2⁺/⁻ mice displayed improved glucose tolerance. In the liver of Tcf7l2⁺/⁻ mice fed on the HFD, reduced lipogenesis and hepatic triglyceride levels were observed when compared with those of wild-type mice. Furthermore, the Tcf7l2⁺/⁻ mice fed on the HFD exhibited decreased peripheral fat deposition. Immunohistochemistry in mouse pancreatic islets showed that endogenous expression of Tcf7l2 was upregulated in the wild-type mice, but not in the Tcf7l2⁺/⁻ mice, after feeding with the HFD. However, the haploinsufficiency of Tcf7l2 in mouse pancreatic islets resulted in little changes in glucose-stimulated insulin secretion.ConclusionThese results suggest that decreased expression of Tcf7l2 confers reduction of diabetic susceptibility in mice via regulation on the metabolism of glucose and lipid."xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.org/dc/terms/identifier | "doi:10.7150/ijbs.4568"xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/author | "Lee J.H."xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/author | "Yang H."xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/author | "Shu Y."xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/name | "Int J Biol Sci"xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/pages | "791-801"xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/title | "Reduction in Tcf7l2 expression decreases diabetic susceptibility in mice."xsd:string |
http://purl.uniprot.org/citations/22719219 | http://purl.uniprot.org/core/volume | "8"xsd:string |
http://purl.uniprot.org/citations/22719219 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22719219 |
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