Effect of Chenodeoxycholic Acid on Serum and Biliary Lipids in Patients with Hyperlipoproteinaemia

Angelin, Bo; Einarsson, Kurt; Leijd, Barbro

doi:10.1042/cs0540451

Cited by 16 publications

(6 citation statements)

References 22 publications

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“…We showed that taurocholate inhibited the disappearance of cellular triacylglycerol; this was observed both if triacylglycerol mass or 3 H in prelabelled triacylglycerols was followed. Two hypotheses may be proposed to explain such a metabolic response to taurocholate.…”

Section: Influence Of Taurocholate On the Intracellular Lipolysis Of mentioning

confidence: 81%

“…Die Geschwindigkeit der Sekretion der Triacylglycerinmasse oder der 3 There is a poorly understood relationship between bile acid and triacylglycerol metabolism. Die Geschwindigkeit der Sekretion der Triacylglycerinmasse oder der 3 There is a poorly understood relationship between bile acid and triacylglycerol metabolism.…”

Section: Gallensäuren Hemmen Die Sekretion Von Very-low-densi(y-lipopmentioning

confidence: 99%

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Bile Acids Inhibit Secretion of Very Low Density Lipoprotein by Rat Hepatocytes

Pozo¹,

Barth²

1987

Biological Chemistry Hoppe-Seyler

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The influence of taurocholate on very low density lipoprotein (VLDL) triacylglycerol synthesis and secretion was studied by isolated rat liver-parenchymal cells. The incorporation of [ 3 H]glycerol into cell-associated and VLDL triacylglycerols were measured after incubation in medium containing 0.75mM oleate. Taurocholate caused a maked decrease in VLDL [ 3 H]triacylglycerol secretion from the hepatocytes: 50-150 taurocholate inhibited secretion of VLDL [ 3 H]triacylglycerols by 70-90%. Similar results were obtained when the mass of secreted VLDL triacylglycerols was measured. Taurocholate caused a decreased secretion of VLDL [ 3 H]triacylglycerols after 15-30 min incubation.A higher amount of cellular triacylglycerols was found in taurocholate-supplemented cells. Furthermore taurocholate did not change the intracellular lipolysis of triacylglycerols. These results suggest that bile acids interfere more probably with the assembly and/ or secretion of VLDL-particles and not with earlier stages of VLDL formation, e.g. triacylglycerol synthesis. Gallensäuren hemmen die Sekretion von Very-Low-Densi(y-Lipoproteinen in isolierten HepatozytenZusammenfassung: Es wurde die Geschwindigkeit der VLDL-Triacylglycerin-Sekretion durch isolierte Hepatozyten der Ratte gemessen. Die Geschwindigkeit der Sekretion der Triacylglycerinmasse oder der 3 H-Aktivität sezernierter VLDL (nach Vormarkierung der zellulären Triacylglycerine mit [ 3 H]Glycerin) zeigten ein Maximum bei 0.75mM Oleat. 50-150 Taurocholat hemmten die Sekretionsgeschwindigkeit von VLDL-[ 3 H]Triacylglycerinen um 70-90%. Ein paralleler Hemmeffekt wurde bei Verfolgung der sezernierten Triacylglycerinmasse beobachtet. Die Hemmung trat innerhalb von 15-30 min ein. Taurocholat führte zu einem gleichzeitigen Anstieg der zellulären Triacylglycerinkonzentration. Es wird gefolgert, daß Gallensäuren in physiologischen Konzentrationen die Sekretion von VLDL-Triacylglycerinen hemmen. Dieses könnte die inverse Beziehung zwischen Gallensäure-Poolgröße und Serumtriacylglycerinspiegeln am Ganztier erklären. Wahrscheinlich greifen Gallensäuren primär eher bei der Assemblierung oder Sekretion der VLDL als bei der Synthese der Triacylglycerine an.

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Section: Influence Of Taurocholate On the Intracellular Lipolysis Of mentioning

confidence: 81%

Section: Gallensäuren Hemmen Die Sekretion Von Very-low-densi(y-lipopmentioning

confidence: 99%

Bile Acids Inhibit Secretion of Very Low Density Lipoprotein by Rat Hepatocytes

Pozo¹,

Barth²

1987

Biological Chemistry Hoppe-Seyler

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“…Another therapeutic possibility in patients with mild hypertriglyceridaemia emerges from studies of the effects of treatment with chenodeoxycholic acid. This might prove to be a useful alternative since this bile acid lowers serum triglyceride levels as well as biliary cholesterol saturation in patients with hyperlipoproteinaemia [35] .…”

Section: Discussionmentioning

confidence: 99%

Biliary lipid composition during treatment with different hypolipidaemic drugs*

Angelin

Einarsson

Leijd

1979

Eur J Clin Investigation

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In an attempt to clarify the possible lithogenic effects of commonly used hypolipidaemic drugs, gallbladder bile was obtained from patients with primary hyperlipoproteinaemia before and during treatment with nicotinic acid (n = 13), cholestyramine (n = 19), clofibrate (n = 11), and a combination of cholestyramine and clofibrate (n = 11). Each treatment period was minimum 6 weeks, and standardized dietary conditions were obtained. Both nicotinic acid and clofibrate treatment caused an increase in biliary cholesterol concentration relative to biliary total lipids (bile acids, phospholipids, and cholesterol). During cholestyramine medication the relative cholesterol concentration fell. A combination of cholestyramine with clofibrate medication led to a decrease of bile saturation to pretreatment levels in nine of the eleven subjects. In the other two a further increase in the cholesterol saturation of the bile occurred. Treatment with nicotinic acid and clofibrate but not with cholestyramine is thus probably associated with an increased risk for development of cholesterol gallstones. It is suggested that addition of cholestyramine may be a possible way to prevent the lithogenic effect of clofibrate in patients with hyperlipoproteinaemia when not only hypocholesterolaemic but also hypotriglyceridaemic effects are wanted.

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“…1), in agreement with some other reports [16,17). Other authors, on the other hand, have observed a reduction of these blood lipids in patients with increased serum cholesterol and triglycerides [18][19][20][21][22].…”

Section: Resultsmentioning

confidence: 99%

Treatment of Radiolucent Gallstones with CDCA or UDCA

Polli¹

1981

Digestion

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Patients with radiolucent gallstones (diameter < 1.5 cm) and functioning gallbladder were treated for 6–12 months with CDCA (38 patients, 12–15 mg/kg/day) or UDCA (78 patients randomly allocated to receive 5–6 or 10–12 mg/kg/day). Complete dissolutions and partial plus complete dissolutions were respectively 26 and 58% for CDCA, 14 and 58% for UDCA at the lower dose, and 29 and 71 % for UDCA at the higher dose. Statistical analysis did not show any significant difference between the three different treatments. In patients with stones of 4–10 mm diameter treated with UDCA, complete dissolution occurred at the lower dose in 0 of 14 cases while complete dissolutions occurred at the higher dose in 5 of 18 cases, suggesting that the latter dose may be more effective (0.05 < p < : 0.1). A highly significant correlation was demonstrated between gallstone size and number of dissolutions with both doses of UDCA. No side effects were observed with UDCA, while with CDCA diarrhea occurred in 28% and a transient increase in SGOT in a single patient. 1 patient on UDCA required emergency cholecystectomy for acute cholecystitis. Dyspeptic and/or pain symptomatology improved in 65 and 85% of the patients treated with CDCA and UDCA, respectively. No variations in blood lipids were observed.

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Effect of Chenodeoxycholic Acid on Serum and Biliary Lipids in Patients with Hyperlipoproteinaemia

Cited by 16 publications

References 22 publications

Bile Acids Inhibit Secretion of Very Low Density Lipoprotein by Rat Hepatocytes

Bile Acids Inhibit Secretion of Very Low Density Lipoprotein by Rat Hepatocytes

Biliary lipid composition during treatment with different hypolipidaemic drugs*

Treatment of Radiolucent Gallstones with CDCA or UDCA

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