Preliminary noteTauroursodeoxycholate and taurochenodeoxycholate stabilize bile lipid metastability through different mechanisms: relation to phospholipid fatty acid composition1
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AbstractLecithin–cholesterol vesicles are present in bile and play a role in cholesterol metastability. Cholesterol holding capacity of vesicles is regulated by lecithin hydrophobicity. In the present study, the effect of therapeutic bile salts on biliary lipid secretion rate and phospholipid fatty acid composition was evaluated in bile duct-fistula rats to determine whether bile salts modulate biliary phospholipid species to, thereby, regulate a physico-chemical metastability of bile cholesterol. Rats were depleted with bile salt pool by overnight biliary diversion and reinfused intravenously with sodium taurocholate (TC) at a constant rate (200 nmol/min per 100 g b.w.) for 3 h, followed by infusion of either sodium taurochenodeoxycholate (TCDC) or tauroursodeoxycholate (TUDC) at a compatible rate. TCDC-infusion increased the biliary secretion rate of cholesterol and phospholipids with a decrease in molar ratio of cholesterol to phospholipid (C/P) when compared to values under TC-infusion, and this was associated with an increase in the molar ratio of phospholipid saturated to unsaturated fatty acids (S/U). In contrast, TUDC-infusion decreased such a biliary lipid secretion rate with an increase in C/P, and this was associated with a decrease in a molar ratio of arachidonate in phospholipids. These findings indicate that TCDC enhances a cholesterol packing density of biliary particulate species by decreasing C/P ratio and increasing S/U, whereas TUDC improves bile lithogenecity by decreasing biliary cholesterol and phospholipid secretion rates and reducing bile arachidonyl phospholipids.

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