First, an insulin-independent model was developed, which possesses clinical phenotype of glycemic response impaired, A1c glycohemoglobin elevated, and dyslipidemia with hypertriglyceridemia and cholesterolemia (VLDL and LDL fractions elevated with HDL decrement), despite hyperinsulinemia present as it happens in type 2 diabetes mellitus. This evidence concerns the gene INS and metabolic syndrome.