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 Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Objective IUGR re-programs hepatic gene expression, leading to alterations in perinatal mRNA levels that persist postnatally. Forkhead bos protein O1a (FoxO1a) is a nclear transcription factor, which is an important regulator of the in vivo metabolism of energetic substance, and play an important role in stabilizing the hepatocyte glucose metabolism and maintaining blood glucose levels in the body. Recent study investigated FoxO1a expression can stimulate key enzymes of gluconeogenesis pathway phosphoenolpyruvate carboxylase kinases (PEPCK), peroxisome proliferator-activated receptor g auxiliary activating factor1a (PGC-1a) and glucose 6 phosphatase (G-6-Pase) gene expression. The effect of IUGR upon hepatic FoxO1a expression is unknown. So in this study we investigate the persistent changes in hepatic FoxO1a expression caused by IUGR, which could initiate and maintain the obesity, insulin resistance and type 2 diabetes, and explore whether the changes in FoxO1a expression are gender specific.

Uteroplacental insufficiency decreases forkhead box protein O1A (foxO1a) hepatic levels in perinatal and postnatal IUGR rats