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4,4 '-Dichlorodiphenyltrichloroethane (DDT) and 4,4 '-dichlorodiphenyldichloroethylene (DDE) inhibit myogenesis in C2C12 myoblasts

Authors
Kim, JonggunPark, Min YoungKim, YooYoon, Kyong SupClark, John MarshallPark, YeonhwaWhang, Kwang-Youn
Issue Date
12월-2017
Publisher
WILEY
Keywords
DDT; DDE; myogenesis; MyoD1; AKT; mTOR
Citation
JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, v.97, no.15, pp.5176 - 5185
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
Volume
97
Number
15
Start Page
5176
End Page
5185
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/81300
DOI
10.1002/jsfa.8399
ISSN
0022-5142
Abstract
BACKGROUNDMost countries have banned the use of 4,4-dichlorodiphenyltrichloroethane (DDT). However, owing to its extremely high lipophilic characteristics, DDT and its metabolite 4,4-dichlorodiphenyldichloroethylene (DDE) are ubiquitous in the environment and in many types of food. The positive correlation between exposure to insecticides, including DDT and DDE, and weight gain, resulting in impaired energy metabolism in offspring following perinatal DDT and DDE exposure, was previously reported. Therefore the influence of DDT and DDE on myogenesis using C2C12 myoblasts was investigated in this study. RESULTSDDT and DDE decreased myotube formation dose- and time-dependently. Among myogenic regulatory factors, DDT and DDE mainly decreased MyoD1 and Myf5 expression. DDT and DDE treatment also altered Myostatin expression, phosphorylation of protein kinase B, p70 ribosomal protein S6 kinase, forkhead box O protein 3 and mammalian target of rapamycin, resulting in attenuation of myotube formation. CONCLUSIONThese results may have significant implications for understanding the effects of developmental exposure of DDT and DDE on myogenesis and development of obesity and type 2 diabetes later in life. (c) 2017 Society of Chemical Industry
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