Duane W C
Department of Medicine, Veterans Affairs Medical Center, Minneapolis, MN 55417.
J Lipid Res. 1995 Jan;36(1):96-107.
To better define the abnormality of bile acid metabolism associated with hypertriglyceridemia, we measured bile acid kinetics and absorption as well as preferential use of newly synthesized cholesterol for bile acid synthesis in eleven controls and ten subjects with hypertriglyceridemia, six of whom could be classified as having familial hypertriglyceridemia (FHT). Fractional turnover rates of cholic acid and chenodeoxycholic acid were both significantly elevated in hypertriglyceridemic subjects to nearly twice the rates in controls. Bile acid synthesis was also significantly higher in hypertriglyceridemic subjects while bile acid pools were either unchanged or somewhat reduced. Consistent with these kinetics, bile acid absorption was significantly lower in hypertriglyceridemic subjects than in controls. Overall only 10-12% of bile acid was derived from newly synthesized cholesterol, and hypertriglyceridemic subjects did not differ from controls. Because hypertriglyceridemia should not alter bile acid absorption, these results are consistent with the previously suggested possibility (B. Angelin, K. S. Hershon, and J. D. Brunzell, 1987. Proc. Natl. Acad. Sci. USA. 84: 5434-5438) that impaired bile acid absorption may be a primary defect in some patients with hypertriglyceridemia.
为了更好地界定与高甘油三酯血症相关的胆汁酸代谢异常,我们测定了11名对照者和10名高甘油三酯血症患者的胆汁酸动力学、吸收情况以及新合成胆固醇用于胆汁酸合成的优先利用情况,其中10名高甘油三酯血症患者中有6名可归类为家族性高甘油三酯血症(FHT)。高甘油三酯血症患者中胆酸和鹅去氧胆酸的分数转换率均显著升高,几乎是对照者的两倍。高甘油三酯血症患者的胆汁酸合成也显著更高,而胆汁酸池要么未变,要么有所减少。与这些动力学情况一致,高甘油三酯血症患者的胆汁酸吸收显著低于对照者。总体而言,只有10 - 12%的胆汁酸来自新合成的胆固醇,高甘油三酯血症患者与对照者并无差异。由于高甘油三酯血症不应改变胆汁酸吸收,这些结果与之前提出的可能性(B. 安格林、K. S. 赫申和J. D. 布伦泽尔,1987年。《美国国家科学院院刊》。84: 5434 - 5438)一致,即胆汁酸吸收受损可能是一些高甘油三酯血症患者的原发性缺陷。