As the major cause of female anovulatory infertility, polycystic ovary syndrome (PCOS) affects a great proportion of women at childbearing age. Although glucagon-like peptide 1 receptor agonists (GLP-IRAs) show therapeutic effects for PCOS, its target and underlying mechanism remains elusive. In the present study, we identified that, both in vivo and in vitro, GLP-1 functioned as the regulator of proliferation and antiapoptosis of MGCs of follicle in PCOS mouse ovary. Furthermore, forkhead box protein O1 (FoxO1) plays an important role in the courses. Regarding the importance of granulosa cells (GCs) in oocyte development and function, the results from the current study could provide a more detailed illustration on the already known beneficial effects of GLP-1RAs on PCOS and support the future efforts to develop more efficient GLP-1RAs for PCOS treatment.
diabetes mellitus is a metabolic disorder predominantly caused by the dysfunction of pancreatic β-cells. This dysfunction is partly caused by the dysregulation of pyruvate dehydrogenase (PdH), which acts as an important mediator of pyruvate oxidation after glycolysis and fuels the tricarboxylic acid cycle. Previous studies have reported decreased PdH expression in rodent models and humans with type 2 diabetes mellitus (T2dM), suggesting that PdH may play an important role in the development of T2dM. However, the mechanism by which PdH affects insulin secretion and β-cell development is poorly understood. Using immunofluorescence staining, the present study found that the expression of pyruvate dehydrogenase e1-α subunit (PdHa1; encoded by the PDHA1 gene) in the islets of type 2 diabetic mice (db/db mice) was lower than in wild-type mice, which indicated the possible association between PdHa1and diabetes. To further understand this mechanism, an inducible, islet-specific PdHa1 knockout mouse (βKo) model was established. The phenotype was authenticated, and the blood glucose levels and islet function between the βKo and control mice were compared. Though no changes were found in food intake, development status, fasting blood glucose or weight between the groups, the level of insulin secretion at 30 min after glucose injection in the βKO group was significantly lower compared with the control group. Furthermore, the performed of the βKo mice on the intraperitoneal glucose tolerance test was visibly impaired when compared with the control mice. Pancreatic tissues were collected for hematoxylin and eosin staining, immunohistochemical and confocal laser-scanning microscopy analysis. examination of the islets from the βKo mouse model indicated that abolishing the expression of PdH caused a compensatory islet enlargement and impaired insulin secretion.
Retraction: [Li‐Hua Zhou, Ya‐Lian Huang, Shu‐Chang Lai, Zong‐Cun Chen, Xian‐Ying Chen, Feng Ju, Mao‐Xiong Fu, Two Cu(II)‐based coordination polymers: Treatment activity on diabetic nephropathy via reducing aldose reductase activity and blood glucose concentration, J. Chin. Chem. Soc. (https://doi.org/10.1002/jccs.202000344)].
The above article, published online on 22 January 2021 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor‐in‐Chief, Jye‐Shane Yang, and Wiley‐VCH GmbH, Weinheim. The retraction has been agreed due to major overlap between this article and the following article published in Polyhedron, "Three Co(II) coordination polymers constructed from 2,5‐di(4‐pyridyl)thiazolo[5,4‐d]thiazole and V‐shaped dicarboxylic acids: Syntheses, characterizations, structural diversity and optical properties" by Mürsel Arıcıa, Okan Zafer Yeşilela, Necmi Degeb, Volume 163 (2019); 77‐83: doi.org/10.1016/j.poly.2019.02.021. Furthermore, investigation of the thermogravimetric and elemental analysis of the materials presented in the article revealed inconsistencies that render the conclusions unreliable.
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