beta-sitosterol: esterification by intestinal acylcoenzyme A: cholesterol acyltransferase (ACAT) and its effect on cholesterol esterification.
beta-sitosterol: esterification by intestinal acylcoenzyme A: cholesterol acyltransferase (ACAT) and its effect on cholesterol esterification.
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发表时间：
1983-04
影响因子：
6.5
通讯作者：
F. Field;S. Mathur
中科院分区：
文献类型：
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作者：
F. Field;S. Mathur
兔子喂食10%椰子油、10%椰子油和1% β-谷甾醇、10%椰子油和1%胆固醇或10%椰子油和1% β-谷甾醇加1%胆固醇4周。来自喂食1% β-谷甾醇饮食的动物的肠的微粒体膜的胆固醇减少48%，并且与来自仅喂食椰子油饮食的动物的膜相比，富含两倍的β-谷甾醇。空回肠中酰基辅酶A：胆固醇酰基转移酶（ACAT）的活性在单独饲喂植物甾醇的动物中显著降低。在喂食1% β-谷固醇和1%胆固醇的动物的细胞膜中，与仅喂食胆固醇的对照组相比，β-谷固醇含量增加了50%，而胆固醇略有下降。与对照组相比，喂食两种固醇的动物的肠道ACAT没有变化。通过将肠微粒体膜与[（14）C] β-谷甾醇-白蛋白乳剂或[（14）C] β-谷甾醇：二棕榈酰磷脂酰胆碱（DPPC）脂质体一起孵育，以放射性标记内源性甾醇库，测定β-谷甾醇酯化。然后加入油酰辅酶A。与使用这两种技术的胆固醇相比，β-谷甾醇的CoA依赖性酯化速率非常慢。在喂食1% β-谷甾醇的动物中，内源性微粒体β-谷甾醇的量增加，不会干扰继发于膜胆固醇富集的ACAT活性刺激。用β-谷甾醇使微粒体膜富集三至五倍并不影响ACAT活性。将新鲜分离的肠细胞与[（3）H]油酸和β-谷甾醇：DPPC或25-羟基胆固醇：DPPC孵育1小时。在β-谷甾醇的存在下，油酸与胆固醇酯的结合没有变化，但在加入25-羟基胆固醇后增加了四倍。我们得出结论，CoA依赖的酯化率的胆固醇是至少60倍以上的β-谷甾醇。膜β-谷甾醇不干扰或竞争胆固醇酯化。这种植物甾醇的酯化不足可能在肠道对β-谷甾醇的吸收不良中发挥作用。Field，F. J.，和S. N.马图尔β-谷甾醇：通过肠酰基辅酶A：胆固醇酰基转移酶（ACAT）酯化及其对胆固醇酯化的影响。
Rabbits were fed either 10% coconut oil, 10% coconut oil and 1% beta-sitosterol, 10% coconut oil and 1% cholesterol, or 10% coconut oil and 1% beta-sitosterol plus 1% cholesterol for 4 weeks. Microsomal membranes from intestines of animals fed the 1% beta-sitosterol diet had 48% less cholesterol and were enriched twofold in beta-sitosterol compared to membranes from animals fed the coconut oil diet alone. Acylcoenzyme A:cholesterol acyltransferase (ACAT) activity in jejunum and ileum was decreased significantly in animals fed the plant sterol alone. In membranes from animals fed 1% beta-sitosterol and 1% cholesterol, beta-sitosterol content increased 50% whereas cholesterol was modestly decreased compared to their controls fed only cholesterol. Intestinal ACAT was unchanged in the animals fed both sterols when compared to their controls. beta-Sitosterol esterification was determined by incubating intestinal microsomal membranes with either [(14)C]beta-sitosterol-albumin emulsion or [(14)C]beta-sitosterol:dipalmitoyl phosphatidylcholine (DPPC) liposomes to radiolabel the endogenous sterol pool. Oleoyl-CoA was then added. The CoA-dependent esterification rate of beta-sitosterol was very slow compared to that of cholesterol using both techniques. An increased amount of endogenous microsomal beta-sitosterol, which occurs in animals fed 1% beta-sitosterol, did not interfere with the stimulation of ACAT activity secondary to cholesterol enrichment of the membranes. Enriching microsomal membranes three- to five-fold with beta-sitosterol did not affect ACAT activity. Freshly isolated intestinal cells were incubated for 1 hour with [(3)H]oleic acid and beta-sitosterol:DPPC or 25-hydroxycholesterol:DPPC. Incorporation of oleic acid into cholesteryl esters did not change in the presence of beta-sitosterol but increased fourfold after the addition of 25-hydroxycholesterol. We conclude that the CoA-dependent esterification rate of cholesterol is at least 60 times greater than that of beta-sitosterol. Membrane beta-sitosterol does not interfere with nor compete with cholesterol esterification. Inadequate esterification of this plant sterol may play a role in the poor absorption of beta-sitosterol by the gut.-Field, F. J., and S. N. Mathur. beta-Sitosterol: esterification by intestinal acylcoenzyme A:cholesterol acyltransferase (ACAT) and its effect on cholesterol esterification.