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Lack of a liver‐specific apolipoprotein (apo)A‐V in bile promotes cholesterol gallstone formation by disrupting biliary cholesterol homeostasis in mice

ApoA‐V is synthesized exclusively by the liver and secreted into the circulation, involving in plasma lipoprotein and lipid metabolism. Although its concentration in human plasma is extremely low (114–258 ng/mL), 1,000 to 10,000‐fold lower than that of apoB‐100 and apoA‐I, respectively, human and mice lacking functional apoA‐V suffer from hypertriglyceridemia. Because our new results found that apoA‐V is also secreted into bile, we hypothesize that it plays an important role in regulating biliary cholesterol metabolism, and its deficiency reduces cholesterol solubility in bile, promoting cholesterol crystallization and gallstone formation.