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J. Lipid Res.
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A more recent version of this article appeared on June 1, 2009 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 5, 2009

Papers In Press, published online ahead of print February 10, 2009
J. Lipid Res., doi:10.1194/jlr.M800491-JLR200
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Submitted on September 15, 2008
Revised on January 22, 2009
Accepted on February 5, 2009

A search for the role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan's partial lipodystrophy mutation

Kari M. Wojtanik, Keith Edgemon, Srikant Viswanadha, Brigette Lindsey, Martin Haulzik, Weiping Chen, George Poy, Marc Reitman, and Constantine Londos

Laboratory of Cellular and Developmental Biology, NIH, NIDDK, Bethesda, MD 20892

Corresponding Author: wojtanikk{at}niddk.nih.gov

In these studies, 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, FPLD2 transgenic mice appear to develop normally, but after several weeks 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.


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D. B. Savage
Mouse models of inherited lipodystrophy
Dis. Model. Mech., November 1, 2009; 2(11-12): 554 - 562.
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