We further observed that HCLD feeding up-regulated both mRNA expressions of Lxrα and Cd36. Since SIRT1 down-regulates the expression of CD36 by inhibiting the activity of LXR43, thus, it is possible that the decreased SIRT1 induced by HCLD could increase the mRNA expression of Cd36, which promoted fatty acid availability to the liver and facilitated much more synthesis of TG and cholesterol ester, and ultimately contributed to more serious hepatic steatosis. The gene discussed is CD36; the disease is fatty liver disease.