Westergaard H, Dietschy J M
J Clin Invest. 1976 Jul;58(1):97-108. doi: 10.1172/JCI108465.
Studies were undertaken to define the mechanism whereby bile acid facilitates fatty acid and cholesterol uptake into the intestinal mucosal cell. Initial studies showed that the rate of uptake (Jd) of several fatty acids and cholesterol was a linear function of the concentration of these molecules in the bulk phase if the concentration of bile acid was kept constant. In contrast, Jd decreased markedly when the concentration of bile acid was increased relative to that of the probe molecule but remained essentially constant when the concentration of both the bile acid and probe molecule was increased in parallel. In other studies Jd for lauric acid measured from solutions containing either 0 or 20 mM taurodeoxycholate and saturated with the fatty acid equaled 79.8+/-5.2 and 120.8+/-9.4 nmol.min(-1).100 mg(-1), respectively: after correction for unstirred layer resistance, however, the former value equaled 113.5+/-7.1 nmol.min(-1).100 mg(-1). Maximum values of Jd for the saturated fatty acids with 12, 16, and 18 carbons equaled 120.8+/-9.4, 24.1+/-3.2, and 13.6+/-1.1 nmol.min(-1).100 mg(-1), respectively. These values essentially equaled those derived by multiplying the maximum solubility times the passive permeability coefficients appropriate for each of these compounds. The theoretical equations were then derived that define the expected behavior of Jd for the various lipids under these different experimental circumstances where the mechanism of absorption was assumed to occur either by uptake of the whole micelle, during interaction of the micelle with an infinite number of sites on the microvillus membrane or through a monomer phase of lipid molecules in equilibrium with the micelle. The experimental results were consistent both qualitatively and quantitatively with the third model indicating that the principle role of the micelle in facilitating lipid absorption is to overcome unstirred layer resistance while the actual process of fatty acid and cholesterol absorption occurs through a monomer phase in equilibrium with the micelle.
开展了多项研究以确定胆汁酸促进脂肪酸和胆固醇进入肠黏膜细胞的机制。初步研究表明，如果胆汁酸浓度保持恒定，几种脂肪酸和胆固醇的摄取速率（Jd）是这些分子在主体相中浓度的线性函数。相反，当胆汁酸浓度相对于探针分子浓度增加时，Jd显著降低，但当胆汁酸和探针分子浓度同时增加时，Jd基本保持恒定。在其他研究中，从含有0或20 mM牛磺脱氧胆酸盐且脂肪酸饱和的溶液中测得的月桂酸Jd分别为79.8±5.2和120.8±9.4 nmol·min⁻¹·100 mg⁻¹：然而，校正未搅动层阻力后，前一个值等于113.5±7.1 nmol·min⁻¹·100 mg⁻¹。含12、16和18个碳的饱和脂肪酸的Jd最大值分别为120.8±9.4、24.1±3.2和13.6±1.1 nmol·min⁻¹·100 mg⁻¹。这些值基本上等于通过将最大溶解度乘以适用于每种化合物的被动渗透系数得出的值。然后推导了理论方程，这些方程定义了在这些不同实验条件下各种脂质Jd的预期行为，其中吸收机制假定通过整个微团的摄取、微团与微绒毛膜上无数位点相互作用或通过与微团处于平衡的脂质分子单体相发生。实验结果在定性和定量上均与第三个模型一致，表明微团在促进脂质吸收中的主要作用是克服未搅动层阻力，而脂肪酸和胆固醇的实际吸收过程通过与微团处于平衡的单体相发生。
