scholarly journals Effects of High-Glucose and High-Fat Condition on Estrogen Receptor- and Sexual Precocity-Related Genes in GT1-7 Cells

2020 ◽  
Vol 26 ◽  
Author(s):  
Shuqin Wang ◽  
Hong Yao ◽  
Lan Ding ◽  
Yiqing Gao ◽  
Pei Wang ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jinghui Zhai ◽  
Lina Tao ◽  
Yueming Zhang ◽  
Huan Gao ◽  
Xiaoyu Qu ◽  
...  

High glucose and high fat are important inducements for the development and progression of diabetic cardiopathy. Salvianolic acid B (SAB), which is the most abundant and bioactive compound in Danshen, attenuates oxidative stress-related disorders, such as cardiovascular diseases, cerebral ischemia, and diabetes. However, the effect of SAB on diabetic cardiopathy is not clear. The aim of study was to investigate the effect and the underlying molecular mechanisms of SAB on diabetic cardiopathy in vitro model. The human umbilical vein endothelial (HUVEC) cells were treated with high glucose (HG, 30 mM) or high fat (palmitic acid, PA, 0.75 mM) in the presence or absence of SAB (100, 200, and 400 mg/L) and incubated for 24 h. We found that HG or PA induced apoptosis of HUVEC cells, while treatment with SAB inhibited the apoptosis. We also found that SAB reversed HG- or PA-induced oxidative stress, apoptosis cell cytokines production, and expression of thioredoxin-interacting protein (TXNIP). Moreover, SAB increased HG- or PA-induced expression of Sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide- (NAD+-) dependent histone deacetylase. Exposure of HUVEC cells to Ex527 (Sirt1 inhibitor) suppressed the effect of SAB on acetyl-p53 and procaspase-3 expressions. In conclusion, the results suggested that SAB could attenuate HUVEC cells damage treated with HG or PA via Sirt1 and might be a potential therapy agent for the diabetic cardiopathy treatment.


Author(s):  
Xuan Wu ◽  
Yunpeng Zhang ◽  
Yixiao Xing ◽  
Bin Zhao ◽  
Cong Zhou ◽  
...  

2016 ◽  
Vol 4 (17) ◽  
pp. e12913 ◽  
Author(s):  
Dale J. Hamilton ◽  
Laurie J. Minze ◽  
Tanvi Kumar ◽  
Tram N. Cao ◽  
Christopher J. Lyon ◽  
...  

2014 ◽  
Vol 46 (07) ◽  
pp. 471-476 ◽  
Author(s):  
D. Ribeiro ◽  
R. Góes ◽  
M. Pinto-Fochi ◽  
S. Taboga ◽  
P.-A. Abrahamsson ◽  
...  

Author(s):  
Lazarus Gilbert ◽  
Alexander Sean ◽  
Kusuma Gabrielle Ophelia ◽  
Wijaya Kevin ◽  
Soetikno Vivian

2020 ◽  
Author(s):  
Livia Lopez-Noriega ◽  
Rebecca Callingham ◽  
Aida Martinez-Sánchez ◽  
Grazia Pizza ◽  
Nejc Haberman ◽  
...  

AbstractLong non-coding RNAs (lncRNAs) are emerging as crucial regulators of β-cell development and function. Consequently, the mis-expression of members of this group may contribute to the risk of type 2 diabetes (T2D). Here, we investigate roles for an antisense lncRNA expressed from the Pax6 locus (annotated as Pax6os1 in mice and PAX6-AS1 in humans) in β-cell function. The transcription factor Pax6 is required for the development of pancreatic islets and maintenance of a fully differentiated β-cell phenotype. Pax6os1/PAX6-AS1 expression was increased in pancreatic islets and β-cell lines at high glucose concentrations, in islets from mice fed a high fat diet, and in those from patients with type 2 diabetes. Silencing or deletion of Pax6os1/PAX6-AS1 in MIN6 cells and EndoC-βH1cells, respectively, upregulated β-cell signature genes, including insulin. Moreover, shRNA-mediated silencing of PAX6-AS1 in human islets not only increased insulin mRNA, but also enhanced glucose-stimulated insulin secretion and calcium dynamics. In contrast, inactivation of Pax6os1 in mice was largely without effect on glucose homeostasis, though female Pax6os1 null mice on high fat diet (HFD) showed a tendency towards enhanced glucose clearance. Together, our results suggest that increased expression of PAX6-AS1 at high glucose levels may contribute to β-cell dedifferentiation and failure in some forms of type 2 diabetes. Thus, targeting PAX6-AS1 may provide a promising strategy to enhance insulin secretion and improve glucose homeostasis in type 2 diabetes.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Sigal Shaklai ◽  
Meital Grafi-Cohen ◽  
Orli Sharon ◽  
Gabi Shefer ◽  
Dalia Somjen ◽  
...  

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