Moreover, the GH-IGF-1–11ß-HSD-1 enzyme interaction is crucial, as both GH and IGF-1 operate as its inhibitor; therefore, any disruption in the activation of either hormone could result in increased production of cortisol, leading to a disruption in circulating glucocorticoid regulation and increasing the severity of both T2DM and obesity. This evidence concerns the gene GH1 and obesity due to melanocortin 4 receptor deficiency.