Skip Navigation



ToxSci Advance Access published online on July 25, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg195
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
75/2/368    most recent
kfg195v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Barnes, D. M.
Right arrow Articles by Kircher, E. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barnes, D. M.
Right arrow Articles by Kircher, E. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received May 10, 2003; accepted July 7, 2003
© 2003 Society of Toxicology

In Vitro Toxicology and Alternative Testing

Effects of Inorganic HgCl2 on Adipogenesis

David M. Barnes 1*, Paul R. Hanlon 2, and Emily A. Kircher 1

1 Department of Animal Sciences, University of Wisconsin-Madison, Madison, WI 53706; Department of Molecular and Environmental Toxicology, University of Wisconsin-Madison, Madison, WI 53706
2 Department of Pharmacology, University of Wisconsin-Madison, Madison, WI 53706; Department of Molecular and Environmental Toxicology, University of Wisconsin-Madison, Madison, WI 53706

* To whom correspondence should be addressed. E-mail: barnes{at}calshp.cals.wisc.edu.


  Abstract

Mercury is a common pollutant that alters glucose metabolism in adipocytes; however, the effect of HgCl2 on differentiating adipocytes and their subsequent metabolic function is not well understood. Two adipocyte models, the 3T3-L1 and C3H10T1/2 (10T1/2) cell lines were differentiated in the presence of HgCl2. To assess the amount of differentiation in a population, markers of differentiation (PPAR{gamma} and GLUT 4 expression, lipid accumulation) and functions of adipocytes (glucose transport and insulin-induced glucose transport) were measured. HgCl2 exposure significantly decreased the number of phenotypic adipocytes and PPAR{gamma} expression in both 3T3-L1 and 10T1/2 cells without effects on cell viability. GLUT 4 was significantly reduced by HgCl2 treatment in 10T1/2 but not 3T3-L1 cells. Exposure to HgCl2 during differentiation increased basal glucose uptake in a dose dependent manner (up to 2.5-fold) and decreased insulin-induced glucose uptake in 3T3-L1 adipocytes. In contrast, HgCl2 had little effect on basal or insulin-induced glucose uptake in 10T1/2 cells, possibly due to their lower insulin responsiveness. We examined the effect of HgCl2 exposure on signaling events involved in differentiation of adipocytes and cellular stress: the phosphorylation of ERK 1/2 and JNK respectively. HgCl2 exposure had no effect on ERK1/2 phosphorylation in either cell line, increased JNK phosphorylation in the 10T1/2 and had no effect on JNK phosphorylation in 3T3-L1 cells. These data indicate HgCl2 exposure can inhibit the differentiation of fibroblasts into adipocytes as well as influence signaling events and the subsequent metabolic activity of differentiated adipocytes.

Key Words: adipocyte, adipogenesis, mercury, differentiation, 3T3-L1, 10T1/2 .


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.