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• W2103143313 startingPage "921" @default.
• W2103143313 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 under acute insulin stimulation, implicating a reduced glucose uptake in the fasting state and a diminished insulin-mediated storage of glucose as glycogen after a meal." @default.
• W2103143313 created "2016-06-24" @default.
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• W2103143313 date "2002-04-01" @default.
• W2103143313 modified "2023-09-27" @default.
• W2103143313 title "The Diabetic Phenotype Is Conserved in Myotubes Established From Diabetic Subjects" @default.
• W2103143313 cites W2019407986 @default.
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• W2103143313 doi "https://doi.org/10.2337/diabetes.51.4.921" @default.
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