These results underscore the MD potential to modulate metabolic outcomes and preserve survival in the presence of diabetes and obesity, although it cannot fully counteract the disease‐driven metabolic dysfunctions likely due to persistent defects in glucose homeostasis (e.g., MD did not counteract diabetes‐induced alterations in GLUT2 and AKT protein levels; data not shown) and/or pancreatic function (not analyzed). The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.