English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Chronic exposure of pancreatic β-cells to high glucose levels results in β-cell dysfunction and death. These effects can be protected by estrogen. The local pancreatic renin-angiotensin system (RAS) has been shown as a novel pathological pathway of high-glucose-induced cell death. The effect of estrogen on pancreatic RAS is still unknown. This study examines whether estrogen protects against pancreatic β-cell death caused by glucotoxicity via a decrease in the pancreatic β-cell RAS pathway. When INS-1 cells were cultured in a high glucose medium, cell death was significantly higher than when the cells were cultured in a basal glucose medium; similarly, there were also higher levels of  AGTR1 and p47    ph    °    x   mRNA, and protein expression. Moreover, the addition of 10 −8  M 17β-estradiol to INS-1 cells cultured in a high glucose medium markedly reduced cell death,  AGTR1  and  p47    ph    °    x   mRNA levels, and protein expression. Similar results were demonstrated in the pancreatic islets. The presence of 10 −8  M 17β-estradiol, losartan, or a combination of both, in a high glucose medium had similar levels of reduction of  p47    ph    °    x   mRNA and protein expression, compared with those cultured in high glucose. Taken together, estrogen protected pancreatic β-cells from high-glucose-induced cell death by reducing the  AGTR1  pathway.

Estrogen attenuates AGTR1 expression to reduce pancreatic β-cell death from high glucose