Many studies conducted in animal and cell models have suggested that aldosterone excess can also impair glucose metabolism by impaired insulin secretion and by increased insulin resistance (IR) at several levels; hepatic glucose production and uptake, and glucose diffusion and uptake into insulin-sensitive tissues through a mineralocorticoid receptor (MR)-dependent and MR-independent mechanism [5,6,7,8,9,10,11,12,13,14]. This evidence concerns the gene INS and Insulin resistance.