CLC number: R714.256
On-line Access: 2020-12-09
Received: 2020-08-04
Revision Accepted: 2020-10-18
Crosschecked: 2020-11-26
Cited: 0
Clicked: 3247
Xuan Zhou, Jia-qi Li, Li-jie Wei, Meng-zhou He, Jing Jia, Jing-yi Zhang, Shao-shuai Wang, Ling Feng. Silencing of DsbA-L gene impairs the PPARγ agonist function of improving insulin resistance in a high-glucose cell model[J]. Journal of Zhejiang University Science B, 2020, 21(12): 990-998.
@article{title="Silencing of DsbA-L gene impairs the PPARγ agonist function of improving insulin resistance in a high-glucose cell model",
author="Xuan Zhou, Jia-qi Li, Li-jie Wei, Meng-zhou He, Jing Jia, Jing-yi Zhang, Shao-shuai Wang, Ling Feng",
journal="Journal of Zhejiang University Science B",
volume="21",
number="12",
pages="990-998",
year="2020",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2000432"
}
%0 Journal Article
%T Silencing of DsbA-L gene impairs the PPARγ agonist function of improving insulin resistance in a high-glucose cell model
%A Xuan Zhou
%A Jia-qi Li
%A Li-jie Wei
%A Meng-zhou He
%A Jing Jia
%A Jing-yi Zhang
%A Shao-shuai Wang
%A Ling Feng
%J Journal of Zhejiang University SCIENCE B
%V 21
%N 12
%P 990-998
%@ 1673-1581
%D 2020
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2000432
TY - JOUR
T1 - Silencing of DsbA-L gene impairs the PPARγ agonist function of improving insulin resistance in a high-glucose cell model
A1 - Xuan Zhou
A1 - Jia-qi Li
A1 - Li-jie Wei
A1 - Meng-zhou He
A1 - Jing Jia
A1 - Jing-yi Zhang
A1 - Shao-shuai Wang
A1 - Ling Feng
J0 - Journal of Zhejiang University Science B
VL - 21
IS - 12
SP - 990
EP - 998
%@ 1673-1581
Y1 - 2020
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2000432
Abstract: )%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>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.
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