NDLI: Enhanced fasting glucose turnover in mice with disrupted action of TUG protein in skeletal muscle.

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Enhanced fasting glucose turnover in mice with disrupted action of TUG protein in skeletal muscle.

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Enhanced fasting glucose turnover in mice with disrupted action of TUG protein in skeletal muscle.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cartee, Gregory D. Löffler, Michael G. Choi, Cheol Soo Gassaway, Brandon M. Belman, Jonathan P. Booth, Carmen J. Castorena, Carlos M. Shulman, Gerald I. Philbrick, Katerina M. Samuel, Varman T. Habtemichael, Estifanos N. Bogan, Jonathan S. Jornayvaz, Francois R. Birkenfeld, Andreas L. Lee, Hui-young Philbrick, William
Description	Author Affiliation: Löffler MG ( Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8020, USA.)
Abstract	Insulin stimulates glucose uptake in 3T3-L1 adipocytes in part by causing endoproteolytic cleavage of TUG (tether containing a ubiquitin regulatory X (UBX) domain for glucose transporter 4 (GLUT4)). Cleavage liberates intracellularly sequestered GLUT4 glucose transporters for translocation to the cell surface. To test the role of this regulation in muscle, we used mice with muscle-specific transgenic expression of a truncated TUG fragment, UBX-Cter. This fragment causes GLUT4 translocation in unstimulated 3T3-L1 adipocytes. We predicted that transgenic mice would have GLUT4 translocation in muscle during fasting. UBX-Cter expression caused depletion of PIST (PDZ domain protein interacting specifically with TC10), which transmits an insulin signal to TUG. Whereas insulin stimulated TUG proteolysis in control muscles, proteolysis was constitutive in transgenic muscles. Fasting transgenic mice had decreased plasma glucose and insulin concentrations compared with controls. Whole-body glucose turnover was increased during fasting but not during hyperinsulinemic clamp studies. In muscles with the greatest UBX-Cter expression, 2-deoxyglucose uptake during fasting was similar to that in control muscles during hyperinsulinemic clamp studies. Fasting transgenic mice had increased muscle glycogen, and GLUT4 targeting to T-tubule fractions was increased 5.7-fold. Whole-body oxygen consumption (VO2), carbon dioxide production (VCO2), and energy expenditure were increased by 12-13%. After 3 weeks on a high fat diet, the decreased fasting plasma glucose in transgenic mice compared with controls was more marked, and increased glucose turnover was not observed; the transgenic mice continued to have an increased metabolic rate. We conclude that insulin stimulates TUG proteolysis to translocate GLUT4 in muscle, that this pathway impacts systemic glucose homeostasis and energy metabolism, and that the effects of activating this pathway are maintained during high fat diet-induced insulin resistance in mice.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	28
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-07-12
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Carrier Proteins Metabolism Glucose Transporter Type 4 Glucose Muscle, Skeletal 3T3-L1 Cells Animals Blood Glucose Carbon Dioxide Genetics Deoxyglucose Fasting Blood Glycogen Hypoglycemic Agents Pharmacology Immunoblotting Insulin Mice Mice, Inbred C57BL Mice, Inbred Strains Mice, Transgenic Drug Effects Oxygen Consumption Protein Transport Proteolysis Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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