Association between Arsenic Suppression of Adipogenesis and Induction of CHOP10 via the Endoplasmic Reticulum Stress Response
作者： Yongyong Hou , Peng Xue , Courtney G. Woods , Xia Wang , Jingqi Fu
DOI: 10.1289/EHP.1205731
关键词:
摘要: Background: There is growing evidence that chronic exposure to inorganic arsenic (iAs) associated with an increased prevalence of type 2 diabetes (T2D). However, the mechanisms for diabetogenic effect iAs are still largely unknown. White adipose tissue (WAT) actively stores and releases energy maintains lipid glucose homeostasis. Objective: We sought determine suppression adipogenesis. Methods: The effects its major metabolites on adipogenesis were determined in 3T3-L1 preadipocytes, mouse adipose-derived stromal-vascular fraction cells (ADSVFCs), human tissue–derived stem (ADSCs). Results: Exposure preadipocytes noncytotoxic levels arsenic, including arsenite (iAs3+, ≤ 5 μM), arsenate (≤ 20 trivalent monomethylated (MMA3+, 1 dimethylated (DMA3+, μM) decreased adipogenic hormone-induced a concentration-dependent manner. In addition, iAs3+, MMA3+, DMA3+ exhibited strong inhibitory primary cultured ADSVFCs ADSCs. Time-course studies revealed inhibition by occurred early stage terminal differentiation was highly correlated induction C/EBP homologous protein (CHOP10), endoplasmic reticulum (ER) stress response protein. Induction CHOP10 reduced DNA-binding activity CCAAT/enhancer-binding β (C/EBPβ), which regulates transcription peroxisome proliferator-activated receptor γ C/EBPα. Conclusions: Low-level MMA3+ trigger ER up-regulate CHOP10, inhibits C/EBPβ transcriptional activity, thus suppressing adipogenesis. Arsenic-induced dysfunctional may be capacity WAT store lipids insulin resistance.
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