APOE and hypertriglyceridemia: This receptor enhances the uptake of TG-rich lipoproteins in an insulin-dependent way through interaction with apoE.[24] Inactivation of LRP1 in liver resulted in a significant HDL-cholesterol (HDL-C) decrease in serum,[25] and previous studies indicate an indirect regulation of LRP1 in HDL-C production.[24] Given that increased level of serum UC is substantially correlated with hypertriglyceridemia and low HDL-C,[13] LRP1 gene may potentially regulate the concentration of serum UC and indirectly play a role in the development of gout.