Serum and lipoprotein sitostanol and non-cholesterol sterols after an acute dose of plant stanol ester on its long-term consumption

Gylling, Helena; Hallikainen, Maarit; Simonen, Piia; Miettinen, Helena E.; Nissinen, Markku; Miettinen, Tatu A.

doi:10.1007/s00394-011-0249-5

Cited by 10 publications

(15 citation statements)

References 24 publications

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“…Liver function tests and serum fibrosis markers analyzed by standard laboratory methods included normalized AST and ALT, Gammaglutamyl-transferase (GGT) (U/L), Bilirubin (μmol/L), Haptoglobin (g/L), alfa2-macroglobulin (g/L), Hyaluronic acid (HA) (ng/ml), amino-terminal propeptide of type III procollagen (PIIINP) (ug/L), Apolipoprotein A1 (g/L) and carboxy-terminal telopeptide of type I collagen (ICTP) and serum cholesterol (mg/100 ml). The non-cholesterol sterols (cholestanol, D8-lathosterol, desmosterol, D7-lathosterol, campesterol, sitosterol, sitostanol, avenasterol and squalene) were analyzed by gas–liquid chromatography (GLC) (Agilent 6890N Network GC System, Agilent Technologies Inc., Wilmington, DE) on a 50-m long Ultra 2 capillary column (5% Phenyl-methyl siloxane) (Agilent Technologies, Wilmington, DE, USA), with 5a-cholestane as internal standard [31], [32].…”

Section: Methodsmentioning

confidence: 99%

A Novel Fibrosis Index Comprising a Non-Cholesterol Sterol Accurately Predicts HCV-Related Liver Cirrhosis

et al. 2014

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Diagnosis of liver cirrhosis is essential in the management of chronic hepatitis C virus (HCV) infection. Liver biopsy is invasive and thus entails a risk of complications as well as a potential risk of sampling error. Therefore, non-invasive diagnostic tools are preferential. The aim of the present study was to create a model for accurate prediction of liver cirrhosis based on patient characteristics and biomarkers of liver fibrosis, including a panel of non-cholesterol sterols reflecting cholesterol synthesis and absorption and secretion. We evaluated variables with potential predictive significance for liver fibrosis in 278 patients originally included in a multicenter phase III treatment trial for chronic HCV infection. A stepwise multivariate logistic model selection was performed with liver cirrhosis, defined as Ishak fibrosis stage 5–6, as the outcome variable. A new index, referred to as Nordic Liver Index (NoLI) in the paper, was based on the model: Log-odds (predicting cirrhosis) = −12.17+ (age×0.11) + (BMI (kg/m2)×0.23) + (D7-lathosterol (μg/100 mg cholesterol)×(−0.013)) + (Platelet count (x109/L)×(−0.018)) + (Prothrombin-INR×3.69). The area under the ROC curve (AUROC) for prediction of cirrhosis was 0.91 (95% CI 0.86–0.96). The index was validated in a separate cohort of 83 patients and the AUROC for this cohort was similar (0.90; 95% CI: 0.82–0.98). In conclusion, the new index may complement other methods in diagnosing cirrhosis in patients with chronic HCV infection.

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Section: Methodsmentioning

confidence: 99%

A Novel Fibrosis Index Comprising a Non-Cholesterol Sterol Accurately Predicts HCV-Related Liver Cirrhosis

et al. 2014

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“…They include studies of VLDL, IDL, and LDL apoprotein (apo) B-100 and HDL apo AI kinetics [ 27 , 28 , 29 ], LDL particle size determination [ 27 , 30 ], analysis of small dense LDL cholesterol concentration [ 25 , 27 , 28 , 31 ], analysis of the concentrations of lipoproteins of different sizes [ 32 , 33 ], and evaluation of LDL lipidomics [ 30 ]. Postprandial lipids have also been evaluated [ 34 , 35 , 36 , 37 ].…”

Section: Lipoprotein Metabolismmentioning

confidence: 99%

“…However, serum campesterol concentration was significantly lowered starting from 6 h postprandially and reflecting the reduced sterol absorption. During long-term use of a large dose of phytostanols, avenasterol was postprandially reduced in chylomicrons [ 36 ] suggesting that chronic absorption inhibition with phytostanols decreases phytosterols in triglyceride-rich lipoproteins.…”

Section: Lipoprotein Metabolismmentioning

confidence: 99%

Phytosterols, Phytostanols, and Lipoprotein Metabolism

2015

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The efficacy of phytosterols and phytostanols added to foods and food supplements to obtain significant non-pharmacologic serum and low density lipoprotein (LDL) cholesterol reduction is well documented. Irrespective of age, gender, ethnic background, body weight, background diet, or the cause of hypercholesterolemia and, even added to statin treatment, phytosterols and phytostanols at 2 g/day significantly lower LDL cholesterol concentration by 8%–10%. They do not affect the concentrations of high density lipoprotein cholesterol, lipoprotein (a) or serum proprotein convertase subtilisin/kexin type 9. In some studies, phytosterols and phytostanols have modestly reduced serum triglyceride levels especially in subjects with slightly increased baseline concentrations. Phytosterols and phytostanols lower LDL cholesterol by displacing cholesterol from mixed micelles in the small intestine so that cholesterol absorption is partially inhibited. Cholesterol absorption and synthesis have been carefully evaluated during phytosterol and phytostanol supplementation. However, only a few lipoprotein kinetic studies have been performed, and they revealed that LDL apoprotein B-100 transport rate was reduced. LDL particle size was unchanged, but small dense LDL cholesterol concentration was reduced. In subjects with metabolic syndrome and moderate hypertriglyceridemia, phytostanols reduced not only non- high density lipoprotein (HDL) cholesterol concentration but also serum triglycerides by 27%, and reduced the large and medium size very low density lipoprotein particle concentrations. In the few postprandial studies, the postprandial lipoproteins were reduced, but detailed studies with apoprotein B-48 are lacking. In conclusion, more kinetic studies are required to obtain a more complete understanding of the fasting and postprandial lipoprotein metabolism caused by phytosterols and phytostanols. It seems obvious, however, that the most atherogenic lipoprotein particles will be diminished.

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“…Therefore, evaluation of the effects of plant sterol and plant stanol consumption on postprandial lipid metabolism is warranted. So far, only three studies have addressed postprandial lipid and lipoprotein responses after plant stanol ester intake [ 11 – 13 ] and 1 study assessed TG lowering after plant sterol esters [ 14 ]. Demonty et al assessed postprandial TG concentrations 4 hours after plant sterol consumption and found lower TG concentrations after a combined intake of fish-oil and plant sterols than after an intake of fish oil alone, suggesting a contribution of plant sterols to the TG-lowering effect of fish oil [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of a Plant Sterol or Stanol Enriched Mixed Meal on Postprandial Lipid Metabolism in Healthy Subjects

Baumgartner

Mensink

2016

PLoS ONE

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BackgroundEvidence is increasing that plant sterols and stanols not only lower fasting serum low-density lipoprotein concentrations, but also those of triglycerides (TG). Insight into effects of these components on postprandial TG metabolism, an emerging risk factor for cardiovascular disease, is missing.ObjectiveOur objective was to examine the 8-hour postprandial response after consuming plant sterol or stanol enriched margarine as part of a mixed meal.MethodsThis postprandial study was part of a randomized crossover study in which 42 subjects consumed plant sterol enriched (3 g/d plant sterols), plant stanol enriched (3 g/d plant stanols), and control margarines for 4 weeks. After each period, subjects consumed a shake enriched with 3g plant sterols (sterol period), 3g plant stanols (stanol period) or no addition (control period). Subjects received a second shake with no addition after 4 hours.ResultsTG and apoB48 incremental areas under the curves (iAUC) of the total (0-8h) and 1st meal response (0-4h) were comparable between the meals and in all age categories (I:18-35y, II:36-52y, III:53-69y). In subjects aged 53-69y, TG iAUC after the 2nd meal (4-8h) was higher in the stanol period as compared with the sterol (63.1±53.0 mmol/L/min; P < 0.01) and the control period (43.2±52.4 mmol/L/min; P < 0.05). ApoB48 iAUC after the 2nd meal was higher after the stanol than after the sterol period (67.1±77.0 mg/L/min; P < 0.05) and tended to be higher than after the control period (43.1±64.5 mg/L/min; P = 0.08) in subjects aged 53-69y. These increased postprandial responses may be due to reduced lipoprotein lipase activity, since postprandial apoCIII/II ratios were increased after stanol consumption compared with the control meal.ConclusionPostprandial TG and apoB48 responses are age-dependently increased after plant stanol consumption, which might be related to a changed clearance of triglyceride-rich lipoproteins.Trial RegistrationClinicalTrials.gov NCT01559428

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Serum and lipoprotein sitostanol and non-cholesterol sterols after an acute dose of plant stanol ester on its long-term consumption

Cited by 10 publications

References 24 publications

A Novel Fibrosis Index Comprising a Non-Cholesterol Sterol Accurately Predicts HCV-Related Liver Cirrhosis

A Novel Fibrosis Index Comprising a Non-Cholesterol Sterol Accurately Predicts HCV-Related Liver Cirrhosis

Phytosterols, Phytostanols, and Lipoprotein Metabolism

Effects of a Plant Sterol or Stanol Enriched Mixed Meal on Postprandial Lipid Metabolism in Healthy Subjects

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