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HERO ID
2816877
Reference Type
Journal Article
Title
Mono(2-ethylhexyl)phthalate accumulation disturbs energy metabolism of fat cells
Author(s)
Chiang, HC; Kuo, YT; Shen, CC; Lin, YH; Wang, SL; Tsou, TC
Year
2016
Is Peer Reviewed?
Yes
Journal
Archives of Toxicology
ISSN:
0340-5761
EISSN:
1432-0738
Publisher
SPRINGER HEIDELBERG
Location
HEIDELBERG
Book Title
Arch Toxicol.
Volume
90
Issue
3
Page Numbers
589-601
Language
English
PMID
25543134
DOI
10.1007/s00204-014-1446-9
Web of Science Id
WOS:000370343000008
URL
https://search.proquest.com/docview/1765924350?accountid=171501
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Abstract
Phthalates are lipophilic and tend to accumulate in adipose tissue, an important regulator of energy balance and glucose homeostasis. The study aimed to determine whether cellular phthalate accumulation influenced fat cell energy metabolism. Following a 3-day treatment with adipogenesis-inducing medium and a 2-day treatment with adipogenesis-maintaining medium, 3T3-L1 cells differentiated into adipocytes in the presence of a phthalate at a clinically relevant concentration (30-300 μM) for another 6 days. Two phthalates, di(2-ethylhexyl)phthalate and di-n-butylphthalate, and their metabolites, mono(2-ethylhexyl)phthalate (MEHP) and mono-n-butylphthalate, were used here. The phthalate treatments caused no marked effect on cytotoxicity and adipogenesis. Only the MEHP-treated adipocytes were found having smaller lipid droplets; MEHP accumulated in cells in a dose- and time-dependent manner. The MEHP-treated adipocytes exhibited significant increases in lipolysis and glucose uptake; quantitative real-time polymerase chain reaction (qPCR) analysis revealed correlated changes in expression of marker genes involved in adipogenesis, lipid metabolism, and glucose uptake. Analysis of oxygen consumption rate (a mitochondrial respiration indicator) and extracellular acidification rate (a glycolysis indicator) indicated a higher energy metabolism in the adipocytes. qPCR analysis of critical genes involved in mitochondrial biogenesis and/or energy metabolism showed that expression of peroxisome proliferator-activated receptor γ coactivator-1α, sirtuin 3, and protein kinase A were significantly enhanced in the MEHP-treated adipocytes. In vitro evidence of MEHP impacts on lipolysis, glucose uptake/glycolysis, and mitochondrial respiration/biogenesis demonstrates that MEHP accumulation disturbs energy metabolism of fat cells.
Keywords
Phthalates; MEHP; Adipocytes; Glucose uptake; Lipolysis; Mitochondria
Tags
IRIS
•
Dibutyl Phthalate (DBP)
Database Searches
Litsearch September 2014 - February 2015
Pubmed
Litsearch Jan 2016 - July 2016
Pubmed
LitSearch Jul 2016 - Jan 2017
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PubMed
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Studies with Supporting Data
Mechanistic and genotoxicity studies
•
Phthalates – Targeted Search for Epidemiological Studies
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Source - Jun 2016 Update (Private)
WOS
Source - Dec 2016 Update (Private)
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Exposure Factors Handbook (Post 2011)
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