Abnormal metabolism flexibility in response to high palmitate concentrations in myotubes derived from obese type 2 diabetic patients

► Mitochondrial content is normal in type 2 diabetic myotubes ► Palmitate oxidation is decreased in type 2 diabetic myotubes compared to control myotubes only in condition of lipid overload ► ACC inactivation by palmitate is impaired in type 2 diabetic myotubes ► AICAR and metformin treatments do not activate AMPK or decrease lipid content in type 2 diabetic myotubes ► Mitochondrial inhibition by antimycin or metformin induce an increase in lipid content in control myotubes.