Expression of hepatic GH receptors is partly dependent on insulin, and in T1D patients, because of the decrease in insulin exported from the portal vein, the stimulation of hepatic synthesis and secretion of IGF1 is also reduced, which leads to negative feedback, and the secretion of GH is continuous, and this alteration of the GH/IGF1 axis also contributes to the development and progression of insulin resistance in patients with T1D. This evidence concerns the gene GH1 and Insulin resistance.