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

摘要

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 precul- tured in increasing insulin concentrations for 4 days and subsequently stimulated acutely by insulin.