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LRP6 Enhances Glucose Metabolism by Promoting TCF7L2-Dependent Insulin Receptor Expression and IGF Receptor Stabilization in Humans
Authors:Rajvir Singh,Renata   Belfort De   Aguiar,Sarita Naik,Sheida Mani,Kamal Ostadsharif,Detlef Wencker,Masoud Sotoudeh,Reza Malekzadeh,Robert   S. Sherwin,Arya Mani
Affiliation:1. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA;2. Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06510, USA;3. Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, USA;4. Shahid Motahari Hospital, Isfahan, Iran;5. Department of Internal Medicine, Cardiology, Hartford Hospital, Hartford, CT 06106, USA;6. Department of Pathology and Laboratory Medicine, Tehran University of Medical Sciences, Tehran, Iran;7. Digestive Disease Research Center, Tehran University of Medical Sciences, Tehran, Iran
Abstract:
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  • Highlights? Nondiabetic LRP6 mutation carriers are hyperinsulinemic and insulin resistant ? IR expression is reduced in skeletal muscles of the LRP6 mutation carriers ? Wnt/LRP6 regulate the insulin receptor and IGFR expression ? The LRP6 mutation reduces TCF7L2-dependent IR expression and enhances mTOR activity
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