The epidemiological studies of the association between iron overload and glucose metabolism showed the prevalence of type 2 diabetes in patients with hereditary hemochromatosis and iron-loading thalassemia, conversely explained by studies of glucose metabolism in the Belgrade rat model [33], which carries the point mutation G185R in the gene for DMT1, responsible for impaired iron uptake and consequent anemia, although associated with iron accumulation both in serum and liver. The gene discussed is SLC11A2; the disease is Tangier disease.