Wnt signaling, de novo lipogenesis, adipogenesis and ectopic fat
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Kangxing Song1, Shuxia Wang1, Mitra Mani2 and Arya Mani1,3
1 Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT
2 Cornell University, Ithaca, NY
3 Department of Genetics, Yale University School of Medicine, New Haven, CT
Arya Mani, email:
Received: October 07, 2014 Accepted: November 14, 2014 Published: November 15, 2014
Wnt signaling is as a major regulator of adipogenesis. It differentially regulates the fate of mesenchymal stem cells (MSC) by promoting osteogenesis and myogenesis, and inhibiting adipogenesis. Its loss of function has been associated with impaired osteogenesis and diverse congenital and adult cardiovascular disorders[3,4]. Our group has identified loss of function mutations in Wnt coreceptor LRP6 that underlie autosomal dominant early onset coronary artery (CAD), osteoporosis and most features of the metabolic syndrome, including high plasma triglyceride and LDL-C, diabetes, hypertension, hyperuricemia and fatty liver disease (unpublished data). Following we will describe our most pertinent findings related to Wnt/LRP6 regulation of de novo lipogenesis and adipogenesis and the role of impaired Wnt signaling in generation of ectopic fat, insulin resistance, elevated plasma lipids and non-alcoholic fatty liver disease (NAFLD).
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