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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M800491-JLR200 on March 19, 2009 Originally published In Press as doi:10.1194/jlr.M800491-JLR200 on February 10, 2009 Originally published In Press as doi:10.1194/jlr.M800491-JLR200 on February 5, 2009

Papers In Press, published online ahead of print June 1, 2009
J. Lipid Res., doi:10.1194/jlr.M800491-JLR200
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Journal of Lipid Research, Vol. 50, 1068-1079, June 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutationboxs

Kari M. Wojtanik1,*, Keith Edgemon2,*, Srikant Viswanadha3,*, Brigette Lindsey4,*, Martin Haluzik5,{dagger}, Weiping Chen3, George Poy§, Marc Reitman6,** and Constantine Londos*

* Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892
{dagger} Mouse Metabolic Core, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892
§ Genomics Core Laboratory, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892
** Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892
2 Present address of K. Edgemon: 2921 Deer Hollow Way #114, Fairfax, VA 22031. e-mail: keith@edgemon.net
3 Present address of S. Viswanadha: Glenmark Research Center, Plot A-607, T.T.C. Industrial Area, MIDC, Mahape, NAVI MUMBAI 400 709. e-mail: srikantv@glenmarkpharma.com
4 Present address of B. Lindsey: 78 Bull Street, Charleston, SC 29401. e-mail: brigette.lindsey@gmail.com
5 Present address of M. Haluzik: Charles University, Department of Medicine, U nemocnice 1, 12808, Prague, Czech Republic. e-mail: mhalu@lf1.cuni.cz
6 Present address of M. Reitman: Merck Research Laboratories, PO Box 2000, RY80M-213, 126 East Lincoln Avenue, Rahway, NJ 07065-0900. e-mail: marc_reitman@merck.com

boxs The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of two figures.

This was work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases intramural program, National Institutes of Health.

Published, JLR Papers in Press, March 19, 2009.

1 To whom correspondence should be addressed. e-mail: wojtanikk{at}niddk.nih.gov

We investigated the role of LMNA in adipose tissue by developing a novel mouse model of lipodystrophy. Transgenic mice were generated that express the LMNA mutation that causes familial partial lipodystrophy of the Dunnigan type (FPLD2). The phenotype observed in FPLD-transgenic mice resembles many of the features of human FPLD2, including lack of fat accumulation, insulin resistance, and enlarged, fatty liver. Similar to the human disease, FPLD-transgenic mice appear to develop normally, but after several weeks they are unable to accumulate fat to the same extent as their wild-type littermates. One poorly understood aspect of lipodystrophies is the mechanism of fat loss. To this end, we have examined the effects of the FPLD2 mutation on fat cell function. Contrary to the current literature, which suggests FPLD2 results in a loss of fat, we found that the key mechanism contributing to the lack of fat accumulation involves not a loss, but an apparent inability of the adipose tissue to renew itself. Specifically, preadipocytes are unable to differentiate into mature and fully functional adipocytes. These findings provide insights not only for the treatment of lipodystrophies, but also for the study of adipogenesis, obesity, and insulin resistance.

Supplementary key words adipocyte differentiation • insulin resistance • lamin A • lamin C • laminopathies • preadipocyte • type 2 diabetes

Abbreviations: FPLD2, FPLD, Familial partial lipodystrophy Dunnigan type; aP2, adipocyte fatty-acid binding protein


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