Liu et al. (2010) have shown that high-molecular-weight chitosan can activate Akt (protein kinase B) to promote GLUT4 translocation in the muscle, so that blood glucose can enter cells for metabolic utilization; it can also inhibit the protein expression of phosphoenolpyruvate carboxykinase (PEPCK) and phosphorylated p38 MAPK and increase the phosphorylated AMPK in the liver, indicating that chitosan can inhibit liver gluconeogenesis and enhance skeletal muscle glucose uptake to improve hyperglycemia [8]. The gene discussed is PCK2; the disease is Hyperglycemia.