INS and Hyperinsulinemia: As a conclusion, our results indicate that, although metabolic alterations, mainly leptin resistance in the BWF1 mice, slow-down the progression of autoimmunity, the presence of hyperinsulinemia and the sustained insulin stimulation of organs that remain insulin-sensitive, such as the liver and potentially the kidneys, facilitates the overexpression and activity of the mTOR system and the appearance of the clinical symptoms of SLE.