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http://purl.uniprot.org/citations/33843164http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33843164http://www.w3.org/2000/01/rdf-schema#comment"Disulfide-bond A oxidoreductase-like protein (DsbA-L) is a molecular chaperone involved in the multimerization of adiponectin. Recent studies have found that DsbA-L is related to metabolic diseases including gestational diabetes mellitus (GDM), and can be regulated by peroxisome proliferator-activated receptor γ (PPARγ) agonists; the specific mechanism, however, is uncertain. Furthermore, the relationship between DsbA-L and the novel adipokine chemerin is also unclear. This article aims to investigate the role of DsbA-L in the improvement of insulin resistance by PPARγ agonists in trophoblast cells cultured by the high-glucose simulation of GDM placenta. Immunohistochemistry and western blot were used to detect differences between GDM patients and normal pregnant women in DsbA-L expression in the adipose tissue. The western blot technique was performed to verify the relationship between PPARγ agonists and DsbA-L, and to explore changes in key molecules of the insulin signaling pathway, as well as the effect of chemerin on DsbA-L. Results showed that DsbA-L was significantly downregulated in the adipose tissue of GDM patients. Both PPARγ agonists and chemerin could upregulate the level of DsbA-L. Silencing DsbA-L affected the function of rosiglitazone to promote the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB)/AKT pathway. Therefore, it is plausible to speculate that DsbA-L is essential in the environment of PPARγ agonists for raising insulin sensitivity. Overall, we further clarified the mechanism by which PPARγ agonists improve insulin resistance."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.org/dc/terms/identifier"doi:10.1631/jzus.b2000432"xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Feng L."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Jia J."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Zhou X."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Zhang J.Y."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Wang S.S."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Li J.Q."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"Wei L.J."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/author"He M.Z."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/name"J Zhejiang Univ Sci B"xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/pages"990-998"xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/title"Silencing of DsbA-L gene impairs the PPARgamma agonist function of improving insulin resistance in a high-glucose cell model."xsd:string
http://purl.uniprot.org/citations/33843164http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/33843164http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/33843164
http://purl.uniprot.org/citations/33843164http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/33843164
http://purl.uniprot.org/uniprot/#_B3KTA6-mappedCitation-33843164http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33843164
http://purl.uniprot.org/uniprot/#_Q2NLC8-mappedCitation-33843164http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33843164
http://purl.uniprot.org/uniprot/#_Q6FII1-mappedCitation-33843164http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33843164
http://purl.uniprot.org/uniprot/#_Q9Y2Q3-mappedCitation-33843164http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33843164
http://purl.uniprot.org/uniprot/B3KTA6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33843164
http://purl.uniprot.org/uniprot/Q9Y2Q3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33843164
http://purl.uniprot.org/uniprot/Q2NLC8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/33843164