In individuals with T1D without complications, the stimulation of total blood flow velocity in the forearm and femoral muscles by physiological postprandial hyperinsulinemia was unchanged, while insulin-stimulated glucose uptake and arteriovenous glucose differences across muscle groups were 40% lower in participants with T1D vs healthy humans, suggesting that a defect in glucose extraction rather than blood flow was responsible for insulin resistance. The gene discussed is INS; the disease is Insulin resistance.