Circulating OCN levels are inversely correlated with plasma glucose levels, fat mass and the extent of metabolic impairment in both animal and human studies.6,34 Furthermore, Ocn-deficient mice (Ocn−/−) exhibit higher adiposity, hyperglycemia, hypoinsulinemia, impaired insulin secretion and sensitivity and are glucose intolerant,6 a metabolic phenotype opposite to that observed in Rptorob−/− mice. The gene discussed is INS; the disease is Hyperglycemia.