Effect of bisphenol A on SOCS-3 and insulin signaling transduction in 3T3-L1 adipocytes
Autor: | Qian‑Qi Liu, Hu-Min Qi, Yue‑E Dai, Wei Chen |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Cancer Research medicine.medical_specialty Insulin Receptor Substrate Proteins medicine.medical_treatment Gene Expression Endocrine Disruptors Biology Biochemistry Mice 03 medical and health sciences Insulin resistance Phenols 3T3-L1 Cells Internal medicine Gene expression Adipocytes Genetics medicine Animals Insulin RNA Messenger Benzhydryl Compounds Molecular Biology Protein kinase B medicine.disease Insulin receptor 030104 developmental biology Endocrinology Oncology Suppressor of Cytokine Signaling 3 Protein biology.protein Molecular Medicine Phosphorylation Signal transduction Proto-Oncogene Proteins c-akt Signal Transduction |
Zdroj: | Molecular Medicine Reports. 14:331-336 |
ISSN: | 1791-3004 1791-2997 |
DOI: | 10.3892/mmr.2016.5224 |
Popis: | 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. |
Databáze: | OpenAIRE |
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