In vitro models of insulin resistance: Mitochondrial coupling is differently affected in liver and muscle cells.

Mitochondrial dysfunction in diabetes is a widely studied topic, but inconsistency in literature data suggests a need for valid and reproducible models that will help to clarify this interaction. We aimed to establish insulin resistance models using chronic high insulin treatment in two cell types: myocytes and hepatocytes, characterise them in terms of mitochondrial function and compare them to the widely used palmitate-induced model of insulin resistance. We found that insulin lowered phosphorylation of Akt while not affecting cell viability, ROS production, mitochondrial morphology or respiration, and caused decrease in mitochondrial coupling only in muscle but not in liver cells.