Nature Genetics
37, 1072 - 1081 (2005)
Published online: 18 September 2005; | doi:10.1038/ng1642
Lymphatic vascular defects promoted by Prox1 haploinsufficiency cause adult-onset obesityNatasha L Harvey1, R Sathish Srinivasan1, 5, Miriam E Dillard1, 5, Nicole C Johnson1, 5, Marlys H Witte3, Kelli Boyd2, Mark W Sleeman4
& Guillermo Oliver11
Department of Genetics and Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee
38105-2794, USA. 2
Animal Resources Center, St. Jude Children's Research Hospital, Memphis, Tennessee
38105-2794, USA. 3
Department of Surgery, University of Arizona College of Medicine, Tucson, Arizona
85724-5063, USA. 4
Regeneron Pharmaceuticals, Inc., Tarrytown, New York
10591-6707, USA. 5
These authors contributed equally to this work.
Correspondence should be addressed to Guillermo Oliver guillermo.oliver@stjude.org Multiple organs cooperate to regulate appetite, metabolism, and glucose and fatty acid homeostasis. Here, we identified and characterized lymphatic vasculature dysfunction as a cause of adult-onset obesity. We found that functional inactivation of a single allele of the homeobox gene Prox1 led to adult-onset obesity due to abnormal lymph leakage from mispatterned and ruptured lymphatic vessels. Prox1 heterozygous mice are a new model for adult-onset obesity and lymphatic vascular disease.
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