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dc.contributor.authorDodd, Garron T-
dc.contributor.authorMichael, Natalie J-
dc.contributor.authorLee-Young, Robert S-
dc.contributor.authorMangiafico, Salvatore P-
dc.contributor.authorPryor, Jack T-
dc.contributor.authorMunder, Astrid C-
dc.contributor.authorSimonds, Stephanie E-
dc.contributor.authorBrüning, Jens Claus-
dc.contributor.authorZhang, Zhong-Yin-
dc.contributor.authorCowley, Michael A-
dc.contributor.authorAndrikopoulos, Sofianos-
dc.contributor.authorHorvath, Tamas L-
dc.contributor.authorSpanswick, David-
dc.contributor.authorTiganis, Tony-
dc.identifier.citationeLife 2018; 7: 238704-
dc.description.abstractHypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. The mechanisms that control such adaptive processes remain unclear. Here we define populations of POMC neurons in mice that are activated or inhibited by insulin and thereby repress or inhibit hepatic glucose production (HGP). The proportion of POMC neurons activated by insulin was dependent on the regulation of insulin receptor signaling by the phosphatase TCPTP, which is increased by fasting, degraded after feeding and elevated in diet-induced obesity. TCPTP-deficiency enhanced insulin signaling and the proportion of POMC neurons activated by insulin to repress HGP. Elevated TCPTP in POMC neurons in obesity and/or after fasting repressed insulin signaling, the activation of POMC neurons by insulin and the insulin-induced and POMC-mediated repression of HGP. Our findings define a molecular mechanism for integrating POMC neural responses with feeding to control glucose metabolism.-
dc.subjectPOMC neurons-
dc.subjectcellular signalling-
dc.subjectglucose metabolism-
dc.subjecthuman biology-
dc.subjectprotein tyrosine phosphatase-
dc.titleInsulin regulates POMC neuronal plasticity to control glucose metabolism.-
dc.typeJournal Article-
dc.typeResearch Support, N.I.H., Extramural-
dc.typeResearch Support, Non-U.S. Gov't-
dc.identifier.affiliationDepartment of Anatomy and Histology, University of Veterinary Medicine, Hungary, Europeen
dc.identifier.affiliationCenter for Endocrinology, Diabetes, and Preventive Medicine, University Hospital Cologne, Cologne, Germanyen
dc.identifier.affiliationExcellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germanyen
dc.identifier.affiliationCenter for Molecular Medicine Cologne, University of Cologne, Cologne, Germanyen
dc.identifier.affiliationNational Center for Diabetes Research, Neuherberg, Germanyen
dc.identifier.affiliationDepartment of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, United Statesen
dc.identifier.affiliationProgram in Integrative Cell Signaling and Neurobiology of Metabolism, Department of Comparative Medicine, Yale University School of Medicine, New Haven, United Statesen
dc.identifier.affiliationMetabolism, Diabetes and Obesity Program, Monash Biomedicine Discovery Institute, Monash University, Melbourne, Australiaen
dc.identifier.affiliationDepartment of Biochemistry and Molecular Biology, Monash University, Victoria, Australiaen
dc.identifier.affiliationDepartment of Physiology, Monash University, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationMonash Metabolic Phenotyping Facility, Monash University, Victoria, Australiaen
dc.identifier.affiliationWarwick Medical School, University of Warwick, Coventry, United Kingdomen
dc.identifier.affiliationDepartment of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germanyen
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