Serum cholestanol, cholesterol precursors, and plant sterols during placebo-controlled treatment of primary biliary cirrhosis with ursodeoxycholic acid or colchicine

Miettinen, Tatu A.; Färkkilä, M.; Vuoristo, Matti; Karvonen, Anna‐Liisa; Leino, Rauli; Lehtola, J; Friman, Claes; Seppälä, K; Tuominen, Juhani

doi:10.1002/hep.1840210508

Cited by 21 publications

(16 citation statements)

References 38 publications

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“…22 However, the magnitude of changes induced by this bile acid in the lipid pattern of patients with PBC is negligible compared with cholesterol-lowering agents. [23][24][25] Moreover, atherosclerosis requires several decades to develop, a period of time that is much longer than the average duration of bile acid treatment in the present PBC series. Finally, it should be noted that in this study each patient with hypercholesterolaemic PBC was matched with a control with hypercholesterolaemia according to a set of criteria that included serum total cholesterol value measured at the time of enrolment.…”

Section: Discussionmentioning

confidence: 99%

Hypercholesterolaemia is not associated with early atherosclerotic lesions in primary biliary cirrhosis

Allocca

Crosignani

Gritti

et al. 2006

Gut

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Section: Discussionmentioning

confidence: 99%

Hypercholesterolaemia is not associated with early atherosclerotic lesions in primary biliary cirrhosis

Allocca

Crosignani

Gritti

et al. 2006

Gut

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“…The new findings in the present study were that UDCA The unchanged esterification percentages of the monotreatment decreased biliary lanosterol and lathosterol levels. methylsterols, esterified by acyl coenzyme A:cholesteryl These cholesterol precursor sterols in serum are considered acyltransferase, 34 and the C-27 noncholesterol sterols (lathreliable indicators of cholesterol synthesis because their seosterols, desmosterol and plant sterols), esterified by lecirum proportions closely reflect the activity of hepatic 3-hythin:cholesterol acyltransferase 35 indicate that in agreement droxy-3-methylglutaryl coenzyme A reductase 30 and the with previous reports, 11,34 UDCA had no effect on these enamount of whole-body cholesterol synthesis. 16,18,19,31,32 Bezymes.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Ursodeoxycholic Acid on Serum and Biliary Noncholesterol Sterols in Patients With Gallstones

1997

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increase in cholesterol synthesis to maintain the body pool Litholytic bile acid ursodeoxycholic acid (UDCA) reof cholesterol unless the decrease in biliary cholesterol secreduces biliary cholesterol secretion and alters cholesterol tion is sufficient to compensate for reduced cholesterol abmetabolism by mechanisms that are not fully undersorption. However, the effect of UDCA on cholesterol metabostood. To evaluate cholesterol metabolism during UDCA lism, especially on cholesterol synthesis, has not been treatment, we studied serum and biliary lipids and choevaluated thoroughly, and the results available are controlesterol precursor sterols (lanosterol and other dimethyl versial, varying from suppression to no effect. 11,13-15 and monomethyl sterols, lathosterols, and desmosterol), Human serum and bile contains, in addition to cholesterol, indicators of cholesterol synthesis, and plant sterols small amounts of noncholesterol sterols, including cholesterol campesterol and sitosterol, indicators of cholesterol abprecursor 16 and dietary plant sterols. 17 Normally and in many sorption, before and during administration of UDCA, 9clinical conditions, the ratios of serum cholesterol precursor mg/kg/d, for 26 weeks in eight patients with radiolucent sterols to cholesterol have been shown to be correlated with gallstones. During UDCA administration, serum lipid the rate of cholesterol synthesis, 16,[18][19][20][21] whereas the serum concentrations were unchanged, but the biliary concenplant sterol levels indicate cholesterol absorption efficiency. 22 tration and molar percentage of cholesterol were markAccordingly, the serum and biliary noncholesterol sterol levedly decreased. The proportions of the cholesterol els might give some additional information on possible precursor sterols to cholesterol were significantly interchanges in cholesterol absorption and synthesis during related between serum and bile before and especially UDCA treatment. To this end we studied the serum and biliduring UDCA administration. Lanosterol and lathosary cholesterol precursor and plant sterol levels in gallstone terol levels, especially in bile, were significantly depatients before and during UDCA treatment to evaluate the creased by 43% and 34%, suggesting that UDCA may ineffects of this treatment on cholesterol absorption and metabhibit cholesterol synthesis. Levels of the other olism. methylase steps, resulting in decreased biliary secretionAfter the baseline studies they started UDCA, 9 mg/kg/d in two daily of cholesterol. Reduced biliary sterol secretion probably doses. Two patients used UDCA for only 4 weeks, whereas the other increased serum plant sterol levels, indicating that un-six patients used it for 6 months. However, 4 weeks' treatment was der these conditions they no longer reflect the intestinal enough to reach metabolic steady-state because in the six long-term efficiency of cholesterol absorption. (HEPATOLOGY patients the biliary molar percentages of cholesterol were similar 1997;25:514-518.) when analyzed after 4 weeks ...

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“…Phytosterol levels have also been investigated in individuals with other health problems such as primary biliary cirrhosis (PBC), a chronic cholestatic liver disease, which progresses from a nonsymptomatic clinical stage, through fibrosis, to endstage liver cirrhosis and finally to death within 10 to 15 years of diagnosis. The ratio of plasma campesterol to sitosterol was found to decrease with progression of this disease (Nikkila et al 1991), perhaps as a result of impaired biliary secretion rather than altered dietary absorption (Miettinen et al 1995b). Two years of drug treatment with ursodeoxycholic acid or colchicine tended to retard the increase in plasma sitosterol levels seen in these patients over time.…”

Section: Typical Plasma Phytosterol Levels In Health and Diseasementioning

confidence: 97%

Dietary phytosterols as cholesterol-lowering agents in humans

Jones¹,

MacDougall²,

Ntanios³

et al. 1997

Can. J. Physiol. Pharmacol.

276

142

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Phytosterols (plant sterols), abundant in fat-soluble fractions of plants, are consumed at levels of 200-400 mg/day in Western diets. Chemically resembling cholesterol, phytosterols inhibit the absorption of cholesterol. Phytosterol consumption in human subjects under a wide range of study conditions has been shown to reduce plasma total and low density lipoprotein (LDL) cholesterol levels; however, the response varies widely. Greater cholesterol-lowering efficacy occurs with consumption of the saturated phytosterol sitostanol versus sitosterol or campesterol. Most studies report no effect of phytosterol administration in high density lipoprotein (HDL) cholesterol or triglyceride levels, although certain evidence exists for an HDL cholesterol raising effect of sitostanol. Phytosterol absorption is limited, although serum phytosterol levels have proven to be important indicators of both cholesterol absorption and synthesis. Serum phytosterols correlate with HDL cholesterol level. In addition, higher phytosterol/cholesterol ratios appear in HDL versus LDL particles, suggesting the existence of an intrinsic phytosterol action, in addition to the extrinsic effect on cholesterol absorption. In conclusion, addition to diet of the phytosterol sitostanol represents an effective means of improving circulating lipid profiles to reduce risk of coronary heart disease.

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Serum cholestanol, cholesterol precursors, and plant sterols during placebo-controlled treatment of primary biliary cirrhosis with ursodeoxycholic acid or colchicine

Cited by 21 publications

References 38 publications

Hypercholesterolaemia is not associated with early atherosclerotic lesions in primary biliary cirrhosis

Hypercholesterolaemia is not associated with early atherosclerotic lesions in primary biliary cirrhosis

The Effects of Ursodeoxycholic Acid on Serum and Biliary Noncholesterol Sterols in Patients With Gallstones

Dietary phytosterols as cholesterol-lowering agents in humans

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