Lee et al. (2007) [4] for the first time highlighted the roles of OCN in glucose metabolism by using OCN knockout (Ocn−/−) mouse models, which showed elevated levels of hyperglycemia and glucose intolerance, decreased β-cell function and insulin secretion, decreased insulin sensitivity and adiponectin expression, and increased fat mass and serum triglyceride level. The gene discussed is BGLAP; the disease is Glucose intolerance.