Next Article in Journal
Psychometric Properties of a 36-Item Version of the “Stress Management Competency Indicator Tool”
Previous Article in Journal
A Comparative Study of Dog- and Cat-Induced Injury on Incidence and Risk Factors among Children
Article Menu

Export Article

Open AccessArticle
Int. J. Environ. Res. Public Health 2016, 13(11), 1085; doi:10.3390/ijerph13111085

Effects of Di-(2-ethylhexyl) Phthalate on Lipid Metabolism by the JAK/STAT Pathway in Rats

1
Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun 130021, China
2
Scientific Research Center, China-Japan Union Hospital, Jilin University, Changchun 130033, China
3
Cancer Center, Tumor Hospital of Jiangxi Province, Nanchang 330029, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: William A. Toscano
Received: 15 August 2016 / Revised: 20 October 2016 / Accepted: 1 November 2016 / Published: 4 November 2016
View Full-Text   |   Download PDF [7956 KB, uploaded 4 November 2016]   |  

Abstract

The most widely used plasticizer, di-(2-ethylhexyl) phthalate (DEHP), is known to affect lipid metabolism and adipogenesis. We studied the effects of dietary DEHP exposure on metabolism in rats as well as the role of the JAK/STAT pathway in this process. Eighty rats were exposed to DEHP (0, 5, 50 and 500 mg/kg/d) through dietary intake for 4 weeks. We then collected blood samples, liver, and adipose tissues to detect modifications in the levels of serum lipids, leptin, adiponectin and insulin. JAK3, STAT5a and PPARγ expression were detected at both the gene and protein levels. The activation of JAK3 and STAT5a was also detected. The DEHP-exposed rats had increased body weight, serum lipid, insulin, and leptin levels. Moreover, the JAK3/STAT5a pathway was activated in the adipose tissue; however, this pathway was not activated in the liver. The mRNA of SREBP-1c in the liver was increased significantly among each of the groups, in contrast to the levels found in the mature SREBP-1c protein form. Furthermore, the expression of FABP4, Acox and FASn was decreased in the liver, but increased in adipose tissue. Thus, we conclude that exposure to DEHP reduces the hydrolysis of lipid and promotes triglyceride accumulation by oppositely regulating the activation state of JAK/STAT pathway in the liver and adipose tissue, resulting in the disorder of body lipid metabolism and obesity. View Full-Text
Keywords: di-(2-ethylhexyl) phthalate; JAK/STAT; lipid metabolism; adipose tissue di-(2-ethylhexyl) phthalate; JAK/STAT; lipid metabolism; adipose tissue
Figures

Figure 1a

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Jia, Y.; Liu, T.; Zhou, L.; Zhu, J.; Wu, J.; Sun, D.; Xu, J.; Wang, Q.; Chen, H.; Xu, F.; Zhang, Y.; Zhang, T.; Liu, H.; Ye, L. Effects of Di-(2-ethylhexyl) Phthalate on Lipid Metabolism by the JAK/STAT Pathway in Rats. Int. J. Environ. Res. Public Health 2016, 13, 1085.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Environ. Res. Public Health EISSN 1660-4601 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top