title: Effect of bisphenol A on SOCS-3 and insulin signaling transduction in 3T3-L1 adipocytes.
abstract: 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.
authors.affiliation: Department of Endocrinology, Nanjing Children's Hospital, Affiliated With Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Yue-E
authors.initials: YE
authors.lastname: Dai
authors.affiliation: Department of Endocrinology, Nanjing Children's Hospital, Affiliated With Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Chen
authors.affiliation: Department of Endocrinology, Nanjing Children's Hospital, Affiliated With Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Humin
authors.initials: H
authors.lastname: Qi
authors.affiliation: Department of Endocrinology, Nanjing Children's Hospital, Affiliated With Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Qian-Qi
authors.initials: QQ
authors.lastname: Liu
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism*; D000818:Animals; D001559:Benzhydryl Compounds / Q000494:pharmacology*; D052244:Endocrine Disruptors / Q000494:pharmacology*; D015870:Gene Expression; D007328:Insulin / Q000378:metabolism*; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D010636:Phenols / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D000071223:Suppressor of Cytokine Signaling 3 Protein / Q000235:genetics / Q000378:metabolism*; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D052244:Endocrine Disruptors; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D010636:Phenols; D051057:Proto-Oncogene Proteins c-akt; D012333:RNA, Messenger; D000071223:Suppressor of Cytokine Signaling 3 Protein; C006780:bisphenol A; D000098826:Bisphenol A Compounds