School of Health Sciences, University of Wollongong, Northfield Avenue, Wollongong, NSW 2522, Australia.
J Clin Lipidol. 2009 May-Jun;3(3):154-8. doi: 10.1016/j.jacl.2009.04.054. Epub 2009 May 5.
Dietary beta-glucans lower the blood concentrations of cholesterol in animals and humans. Recent studies have uncovered mechanisms by which dietary beta-glucans may regulate cholesterol homeostasis. There is evidence that beta-glucans sequester bile acids in the intestine, reducing their reabsorption and return to the liver. Reducing hepatic bile acid concentrations activates the enzyme CYP7A1, which converts cholesterol into bile acids. This action leads to a reduction of hepatic cell cholesterol content, which up-regulates low-density lipoprotein (LDL) receptor synthesis and thereby accelerates the transportation of LDL-cholesterol from the blood into hepatocytes. Reduced intracellular cholesterol also up-regulates the hepatic synthesis of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol synthesis. Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase and could therefore provide an additive effect in suppressing hepatocyte cholesterol to that produced by enhancing its depletion with beta-glucans. Through this combination of agents, one would expect a greater clearance of LDL from the plasma with lower steady state levels of LDL-cholesterol.
膳食β-葡聚糖可降低动物和人类血液中的胆固醇浓度。最近的研究揭示了膳食β-葡聚糖可能调节胆固醇稳态的机制。有证据表明，β-葡聚糖可在肠道中螯合胆汁酸，减少其重吸收并返回肝脏。降低肝内胆汁酸浓度会激活酶 CYP7A1，将胆固醇转化为胆汁酸。这一作用导致肝细胞膜胆固醇含量降低，从而上调低密度脂蛋白（LDL）受体的合成，加速 LDL-胆固醇从血液进入肝细胞。细胞内胆固醇减少也会上调肝内 3-羟-3-甲基戊二酰辅酶 A 还原酶的合成，该酶是胆固醇合成的限速酶。他汀类药物抑制 3-羟-3-甲基戊二酰辅酶 A 还原酶，因此可能会增强β-葡聚糖对肝细胞胆固醇的耗竭作用，从而产生额外的抑制作用。通过这种联合用药，预计 LDL 从血浆中的清除率会增加，而 LDL-胆固醇的稳态水平会降低。
