Open AccessEffect of bisphenol A on SOCS-3 and insulin signaling transduction in 3T3-L1 adipocytes
Author(s) -
Yutian Dai,
Wei Chen,
Hu-Min Qi,
Qianqi Liu
Publication year - 2016
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2016.5224
Subject(s) - protein kinase b , signal transduction , medicine , biology , endocrinology , insulin receptor , 3t3 l1 , insulin , blot , oncogene , suppressor of cytokine signalling , insulin resistance , microbiology and biotechnology , cell cycle , apoptosis , socs3 , adipose tissue , biochemistry , adipogenesis , gene , stat3
The aim of the present study was to investigate whether environmental endocrine disrupting chemical, bisphenol A (BPA), affects secretion of suppressor of cytokine signaling 3 (SOCS-3) and insulin signaling transduction in 3T3-L1 adipocytes. 3T3-L1 adipocytes were treated for 0, 2, 6, 12 and 24 h with BPA at 80 µM in serum‑deprived medium. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to detect the mRNA expression levels of SOCS‑3 and protein expression levels of SOCS‑3, insulin receptor substrate 1 (IRS‑1), phosphorylated (p)‑IRS‑1, Akt and p‑Akt. The levels of p‑IRS‑1, Akt and p‑Akt in cultures treated for 6 h with BPA were also analyzed by immunofluorescence. The SOCS‑3 mRNA and protein expression levels were decreased in the 6, 12 and 24 h groups. The levels of p‑IRS‑1 and p‑Akt protein were markedly downregulated, while the level of IRS‑1 and Akt protein remained unaltered among these groups, which was consistent with the results observed using immunofluorescence. BPA may inhibit insulin signal transduction and result in the occurrence of insulin resistance via promoting the expression of SOCS-3.