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Estrogenic chemicals at body burden levels attenuate energy metabolism in 3T3‐L1 adipocytes
Author(s) -
Tsou TsuiChun,
Yeh SzuChing,
Hsu JhihWei,
Tsai FengYuan
Publication year - 2017
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3508
Subject(s) - endocrinology , medicine , estrogen receptor , xenoestrogen , downregulation and upregulation , estrogen , endocrine disruptor , chemistry , kinase , mapk/erk pathway , diethylstilbestrol , phthalate , metabolism , nonylphenol , biology , hormone , biochemistry , endocrine system , organic chemistry , cancer , breast cancer , gene , environmental chemistry
Abstract The study aimed to examine effects of environmental estrogens at body burden levels on energy metabolism in fat cells. Acclimation of T47D‐KBluc cells in estrogen‐deprived medium was established for high performance of estrogen‐responsive luciferase reporter assay. With the assay, relative estrogenic potency of four selected estrogen receptor (ER) agonists, i.e. diethylstilbestrol, β‐estradiol, 4‐nonylphenol and bisphenol A, were determined. Immunoblot analysis revealed that the ER agonists at both EC 80 and EC 100 caused rapid and transient phosphorylation of extracellular signal‐regulated kinases (ERK) in an ER‐dependent manner. 3T3‐L1 adipocytes treated with the ER agonists at EC 80 for 24 hours exhibited significant downregulation in mitochondrial respiration and glycolytic function. Importantly, EC 80 values of 4‐nonylphenol (6.0 × 10 −10 m ) and bisphenol A (1.0 × 10 −8 m ) are in the range of human body burdens. The finding that estrogenic chemicals at body burden levels cause significant impact on fat cell energy metabolism raises an important public health issue that deserves more attention.