Thus, <i>PIK3R1</i> C-terminal mutations impair insulin signaling only in some cellular contexts and produce a subphenotype of insulin resistance resembling INSR dysfunction but unlike AKT2 dysfunction, implicating PI3K in the pathogenesis of key components of the metabolic syndrome.
The present work was aimed to identify, does BER-chloride has a poisonous influence on the liver? and investigating the outcome of BER-chloride on PI3K/Akt-p/SIRT-1/PTEN pathway during insulin resistance syndrome.
The down-regulated targets of miR-1207-5p and -129-2-3p were enriched in PI3K and MAPK pathways and 8 out of the 12 enriched pathways were down-regulated in individuals with MetS.
The underlying mechanism was attenuation of the reduced expression of PI3K p85 mRNA and IRS1 protein in both insulin-resistant HepG2 cells and MS rats.