The diabetic phenotype is conserved in myotubes established from diabetic subjects: evidence for primary defects in glucose transport and glycogen synthase activity

Diabetes
M GasterHenning Beck-Nielsen

Abstract

The most well-described defect in the pathophysiology of type 2 diabetes is reduced insulin-mediated glycogen synthesis in skeletal muscles. It is unclear whether this defect is primary or acquired secondary to dyslipidemia, hyperinsulinemia, or hyperglycemia. We determined the glycogen synthase (GS) activity; the content of glucose-6-phosphate, glucose, and glycogen; and the glucose transport in satellite cell cultures established from diabetic and control subjects. Myotubes were precultured in increasing insulin concentrations for 4 days and subsequently stimulated acutely by insulin. The present study shows that the basal glucose uptake as well as insulin-stimulated GS activity is reduced in satellite cell cultures established from patients with type 2 diabetes. Moreover, increasing insulin concentrations could compensate for the reduced GS activity to a certain extent, whereas chronic supraphysiological insulin concentrations induced insulin resistance in GS and glucose transport activity. Our data suggest that insulin resistance in patients with type 2 diabetes comprises at least two important defects under physiological insulin concentrations: a reduced glucose transport under basal conditions and a reduced GS activity un...Continue Reading

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Citations

Jun 12, 2013·Cell and Tissue Research·Vigdis AasArild C Rustan
Dec 4, 2008·Endocrine·Paul S PhillipsUNKNOWN Scripps Mercy Clinical Research Center
Sep 10, 2003·Best Practice & Research. Clinical Endocrinology & Metabolism·Henning Beck-NielsenMichael Gaster
Oct 26, 2011·International Journal of Obesity : Journal of the International Association for the Study of Obesity·K E BoyleJ A Houmard
Oct 16, 2008·The Journal of Clinical Endocrinology and Metabolism·Theodore P CiaraldiRobert R Henry
Nov 6, 2003·Clinical Chemistry and Laboratory Medicine : CCLM·Peter Vollenweider
Jun 15, 2014·Mitochondrion·M Adeva-AndanyJ Rodríguez-Seijas
Oct 6, 2010·Biochemical and Biophysical Research Communications·Ariane D Minet, Michael Gaster
Nov 10, 2009·Molecular and Cellular Endocrinology·Céline AguerMagali Kitzmann
Jun 10, 2009·Molecular and Cellular Endocrinology·T P CiaraldiR R Henry
Jul 21, 2009·Biochemical and Biophysical Research Communications·Michael Gaster
Jan 1, 2007·Obesity Research & Clinical Practice·A J McAinchD Cameron-Smith
Feb 3, 2007·Molecular and Cellular Endocrinology·P CavuotoG A Wittert
Sep 24, 2005·European Journal of Clinical Investigation·B M AbdallahM Gaster
Oct 21, 2003·Journal of Cellular Physiology·Anna SoliniFrancesco Di Virgilio
Jun 15, 2004·Biochemical and Biophysical Research Communications·Michael GasterHenning Beck-Nielsen
Jan 31, 2006·Biochimica Et Biophysica Acta·Michael Gaster, Henning Beck-Nielsen
Mar 28, 2009·Biochemical and Biophysical Research Communications·Michael Gaster
Oct 24, 2014·Journal of Cellular and Molecular Medicine·Pascal PomièsMaurice Hayot
Apr 17, 2012·Biochemistry Research International·Michael Gaster
Jun 16, 2015·BioMed Research International·Shin FujimakiTomoko Kuwabara

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