INTESTINAL TRANSIT, DEOXYCHOLIC-ACID AND THE CHOLESTEROL SATURATION OF BILE - 3 INTER-RELATED FACTORS

INTESTINAL TRANSIT, DEOXYCHOLIC-ACID AND THE CHOLESTEROL SATURATION OF BILE - 3 INTER-RELATED FACTORS
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DOI:
10.1136/gut.27.5.550
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发表时间:
1986-05-01
期刊:
GUT
影响因子:
24.5
通讯作者:
HEATON, KW
HEATON, KW
中科院分区:
医学1区
文献类型:
--
作者:
MARCUS, SN;HEATON, KW

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有大量证据表明胆汁中脱氧胆酸的水平影响胆汁胆固醇饱和度。脱氧胆酸在结肠中形成并缓慢吸收。因此,结肠传输率的变化可能会影响胆汁脱氧胆酸和胆汁中的胆固醇饱和度。当 14 名便秘受试者服用标准化番泻叶片剂六周,剂量足以将平均全肠道转运时间从 134 小时降低至 54 小时时,脱氧胆酸在胆汁胆汁酸中的比例从 25.9.+- 下降。 8.6 至 17.2.+-。 8.3% (p < 0.0001),通过同位素稀释测量的脱氧胆酸池从 0.64 .+/- 下降。 0.34 至 0.45.+-。 0.29 克(p < 0.0001)。在那些胆汁最初胆固醇过饱和的受试者 (n = 8) 中,饱和指数从 1.40 .+- 下降。 0.22 至 1.20.+-。 0.19(p = 0.02)。相反,当 12 名正常志愿者服用足以引起症状性便秘并将平均通过时间从 48 小时延长至 103 小时的洛哌丁胺胶囊时,脱氧胆酸池从 0.40.+- 增加。 0.24 至 0.57.+-。 0.17 克(p = 0.008)。脱氧胆酸百分比没有显着变化,因为估计的总胆汁酸池扩大(从 1.98 .+-. 0.61 到 2.81 .+-. 0.48g;p < 0.081),大概是因为洛哌丁胺减慢了小肠转运。尽管胆汁酸池扩大,洛哌丁胺仍将胆固醇饱和指数从 1.10.+- 增加。 0.31 至 1.20.+-。 0.32(p = 0.01)。结肠传输率的变化会改变脱氧胆酸库的大小和胆汁胆固醇饱和度。这些发现表明,便秘或结肠传输缓慢可能会增加胆汁过饱和的风险,从而增加胆结石的风险。
There is considerable evidence that the level of deoxycholic acid in the bile influences biliary cholesterol saturation. Deoxycholic acid is formed in the colon and absorbed slowly. Hence changes in colonic transit rate might influence biliary deoxycholic acid and the cholesterol saturation of bile. When 14 constipated subjects took standardised senna tablets for six weeks in a dose sufficient to lower mean whole gut transit time from 134 to 54 hours, deoxycholic acid as a proportion of biliary bile acids fell from 25.9 .+-. 8.6 to 17.2 .+-. 8.3% (p < 0.0001) and deoxycholic acid pool measured by isotope dilution fell from 0.64 .+-. 0.34 to 0.45 .+-. 0.29 g (p < 0.0001). In those subjects (n = 8) whose bile was initially supersaturated with cholesterol, the saturation index fell from 1.40 .+-. 0.22 to 1.20 .+-. 0.19 (p = 0.02). Conversely, when 12 normal volunteers took loperamide capsules sufficient to cause symptomatic constipation and to prolong mean transit-time from 48 to 103 hours, the deoxycholic acid pool increased from 0.40 .+-. 0.24 to 0.57 .+-. 0.17 g (p = 0.008). The percentage deoxycholic acid did not alter significantly, because the estimated total bile acid pool expanded (from 1.98 .+-. 0.61 to 2.81 .+-. 0.48g; p < 0.081), presumably because of loperamide slowing down small bowel transit. Despite this expansion of the bile acid pool, loperamide increased the cholesterol saturation index from 1.10 .+-. 0.31 to 1.20 .+-. 0.32 (p = 0.01). Changes in colonic transit rate alter the size of the deoxycholic acid pool and bile cholesterol saturation. These findings suggest that constipation or slow colonic transit might increase the chance of supersaturated bile and hence of gall stones.