Ginter E
Ann N Y Acad Sci. 1975 Sep 30;258:410-21. doi: 10.1111/j.1749-6632.1975.tb29299.x.
Latent chronic ascorbic acid deficiency provokes in guinea pigs a metabolic disorder in the liver, causing an impaired cholesterol transformation to its principal catabolic product, bile acids. This metabolic disorder induces hypercholesterolemia and accumulation of cholesterol in the liver and slows the release of cholesterol from the circulation. Ascorbic acid probably intervenes into the biosynthesis of bile acids at the stage of 7 alpha-hydroxylation of the cholesterol nucleus. High doses of ascorbic acid significantly stimulate cholesterol transformation to bile acids in guinea pigs and decrease plasma cholesterol concentration in humans.
潜在的慢性抗坏血酸缺乏会在豚鼠体内引发肝脏代谢紊乱，导致胆固醇向其主要分解代谢产物胆汁酸的转化受损。这种代谢紊乱会诱发高胆固醇血症以及胆固醇在肝脏中的蓄积，并减缓胆固醇从循环系统中的释放。抗坏血酸可能在胆固醇核7α-羟化阶段介入胆汁酸的生物合成过程。高剂量的抗坏血酸能显著刺激豚鼠体内胆固醇向胆汁酸的转化，并降低人体血浆胆固醇浓度。
