Through an assessment of liver and muscle insulin sensitivity, intramuscular lipid and triglyceride content in muscle cells, whole-body and subcutaneous lipolysis incidence, as well as mitochondrial oxidative phosphorylation activity in muscle, it was determined that a genetic defect in mitochondrial oxidative phosphorylation among T2DM patients results in dysregulation of skeletal muscle IR and intramuscular fatty acid metabolism in the offspring with IR. This evidence concerns the gene INS and type 2 diabetes mellitus.