Connor W E, Lin D S
J Clin Invest. 1974 Apr;53(4):1062-70. doi: 10.1172/JCI107643.
The incomplete absorption of dietary cholesterol may represent an adaptive intestinal barrier that prevents hypercholesterolemia. To explore this mechanism, we compared cholesterol absorption in 15 normocholesterolemic and 6 hypercholesterolemic (type II) subjects fed background cholesterol-free formula diets with 40% of calories as fat. Each test meal consisted of a breakfast into which was incorporated scrambled egg yolk containing 300-500 mg of cholesterol and [4-(14)C]cholesterol (3-22 muCi), either naturally incorporated into the yolk cholesterol by previous isotope injection into the laying hen or added in peanut oil to the yolk of the test breakfast. In some instances [1alpha-(3)H]cholesterol was the radioactive marker. The radioactivity of the fecal neutral sterol fraction was determined in daily stool samples for the next 7 days to provide an estimate of unabsorbed dietary cholesterol. The amount of absorbed and reexcreted labeled cholesterol proved negligible. Most unabsorbed dietary cholesterol appeared in the stool on the second or third day after the meal, and 95% or more was recovered in the stool by 6 days. Plasma specific activity curves were usually maximal at 48 h. Normal subjects absorbed 44.5+/-9.3 (SD) of the administered cholesterol (range 25.9-60.3). Hypercholesterolemics absorbed the same percentage of cholesterol as normals: 47.6+/-12.6% (range 29.3-67.3). Absorption was similar whether the radiolabeled cholesterol was added to egg yolk or naturally incorporated in it (42.1+/-9.3 vs. 48.9+/-9.8%). Six normal subjects were fed a cholesterol-free formula for 4 wk, and then different amounts of cholesterol (110-610 mg/day) were added for another 4 wk. At the end of each period, single test meals containing either 110, 310, or 610 mg of cholesterol and [1alpha-(3)H]cholesterol were administered. Cholesterol absorption was 42.3+/-6.0% and 45.4+/-8.3% for the two dietary periods, respectively. The absolute cholesterol absorption was linearly related to the amount of cholesterol in the test meal, and absorption was not affected by background diets high or low in cholesterol content.
膳食胆固醇吸收不完全可能代表一种适应性肠道屏障,可预防高胆固醇血症。为探究这一机制,我们比较了15名正常胆固醇水平受试者和6名高胆固醇血症(II型)受试者的胆固醇吸收情况,这些受试者食用不含胆固醇的基础配方饮食,其中40%的热量来自脂肪。每次测试餐包括一份早餐,早餐中加入了含有300 - 500毫克胆固醇和[4-(14)C]胆固醇(3 - 22微居里)的炒蛋黄,[4-(14)C]胆固醇要么是之前通过向产蛋母鸡注射同位素自然整合到蛋黄胆固醇中的,要么是在测试早餐的蛋黄中添加到花生油里的。在某些情况下,[1α-(3)H]胆固醇是放射性标记物。在接下来7天的每日粪便样本中测定粪便中性固醇部分的放射性,以估算未吸收的膳食胆固醇。吸收和再排泄的标记胆固醇量可忽略不计。大部分未吸收的膳食胆固醇在餐后第二天或第三天出现在粪便中,到第6天时,95%或更多的胆固醇在粪便中被回收。血浆比活度曲线通常在48小时达到最大值。正常受试者吸收了所给予胆固醇的44.5±9.3(标准差)(范围为25.9 - 60.3)。高胆固醇血症患者吸收的胆固醇百分比与正常人相同:47.6±12.6%(范围为29.3 - 67.3)。无论放射性标记的胆固醇是添加到蛋黄中还是自然整合到蛋黄中,吸收情况相似(42.1±9.3%对48.9±9.8%)。6名正常受试者先食用不含胆固醇的配方饮食4周,然后再添加不同量的胆固醇(110 - 610毫克/天),持续4周。在每个阶段结束时,给予含有110、310或610毫克胆固醇和[1α-(3)H]胆固醇的单次测试餐。两个饮食阶段的胆固醇吸收分别为42.3±6.0%和45.4±8.3%。绝对胆固醇吸收与测试餐中的胆固醇量呈线性相关,且吸收不受胆固醇含量高或低的基础饮食的影响。