scholarly journals Role of the liver in low-density-lipoprotein catabolism in the rat

1984 ◽  
Vol 220 (1) ◽  
pp. 333-336 ◽  
Author(s):  
S Bhattacharya ◽  
S Balasubramaniam ◽  
L A Simons
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Fold Increase ◽  
Hepatic Uptake ◽  
Linear Increase ◽  
Cholesterol Concentration ◽  
Synthesis Rate ◽  
Low Density ◽  
Oestradiol Treatment

Plasma low-density-lipoprotein (LDL) kinetics and hepatic LDL uptake were studied in the rat after an intravenous pulse injection of [14C]sucrose-labelled LDL. Some 96% of injected radioactivity was associated with apoprotein B of LDL (d 1.020-1.050). The disappearance of labelled LDL from plasma was accompanied by a linear increase in the hepatic uptake of LDL, up to 12 h after injection. Oestradiol treatment lowered plasma cholesterol concentration by 58% and the intravascular pool of LDL by 78%. This was associated with a 4-fold increase in the fractional catabolic rate of LDL and a 2-fold increase in the hepatic uptake of LDL. Oestradiol treatment did not significantly change the synthesis rate of LDL; it decreased the skin and lung uptake of LDL, but increased adrenal uptake. These results suggest that the liver plays an important role in the regulation of plasma LDL concentration.

Plasma lipoprotein profiles of normocholesterolemic and hypercholesterolemic homozygotes for apolipoprotein E2(Arg158-->Cys) compared

1994 ◽  
Vol 40 (8) ◽  
pp. 1559-1566 ◽  
Author(s):  
S P Zhao ◽  
A H Smelt ◽  
A M Van den Maagdenberg ◽  
A Van Tol ◽  
T F Vroom ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoprotein ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Plasma Cholesteryl Ester ◽  
Familial Dysbetalipoproteinemia ◽  
Lipoprotein Profiles

Abstract We compared plasma lipoprotein profiles of 15 individuals with normocholesterolemic (plasma cholesterol 4.81 +/- 0.90 mmol/L) familial dysbetalipoproteinemia (NFD) and 15 patients with hypercholesterolemic (plasma cholesterol 10.61 +/- 2.32 mmol/L) familial dysbetalipoproteinemia (HFD), matched for age and sex. All subjects were homozygous for apoE2(Arg158-->Cys). Compared with 15 normolipidemic controls (plasma cholesterol 5.47 +/- 0.92 mmol/L), subjects with NFD and HFD had greater cholesterol concentrations of large very-low-density lipoprotein (VLDL1), small VLDL (VLDL2), and intermediate-density lipoprotein, each of which was correlated to their plasma total cholesterol concentration. VLDL1 and VLDL2 subfractions were enriched in cholesteryl ester, and plasma cholesteryl ester transfer protein activities were increased in both NFD and HFD; however, absolute changes were larger in HFD than in NFD. Concentrations of low-density lipoprotein cholesterol were lower in HFD (1.89 +/- 0.48 mmol/L) and NFD (1.56 +/- 0.36 mmol/L) than in normolipidemic controls (3.35 +/- 0.73 mmol/L). We conclude that all subjects homozygous for apoE2(Arg158-->Cys) show features of dysbetalipoproteinemia.

Platelet Aggregation and Plasma Lipoproteins in Alcoholics During Alcohol Withdrawal

1986 ◽  
Vol 55 (02) ◽  
pp. 173-177 ◽  
Author(s):  
K Desai ◽  
J S Owen ◽  
D T Wilson ◽  
R A Hutton
Keyword(s):  
Platelet Aggregation ◽  
Alcohol Withdrawal ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Plasma Lipoprotein ◽  
Cholesterol Concentration ◽  
Arachidonic Acid Content ◽  
Low Density

SummaryPlatelet aggregation, platelet lipid composition and plasma lipoprotein concentrations were measured each week in a group of seventeen alcoholics, without overt liver disease, for one month, following acute, total alcohol withdrawal. The platelets were initially hypoaggregable but, within 1-2 weeks of cessation of drinking, they became hyperaggregable and then gradually returned towards normal values. Hyperaggregability could not be explained by increases in either the cholesterol or the arachidonic acid content of the platelets. Plasma very-low-density lipoprotein cholesterol levels remained high throughout the study, but the initially raised levels of high-density lipoprotein (HDL) cholesterol fell by 26%. Low-density lipoprotein (LDL) cholesterol concentration rose by 10% after two weeks of withdrawal but then returned to about the starting level. The resulting changes in the plasma LDL-cholesterol: HDL-cholesterol ratio, which had increased by more than 50% after two weeks of abstinence, essentially paralleled the time course of enhanced platelet reactivity in all but four of the alcoholics. These findings suggest that alterations in plasma lipoprotein concentrations during acute alcohol withdrawal may be a contributory factor to the haemostatic disorders present in such patients.

scholarly journals Lipoprotein Signatures of Cholesteryl Ester Transfer Protein and HMG-CoA Reductase Inhibition

2018 ◽  
Author(s):  
Johannes Kettunen ◽  
Michael V. Holmes ◽  
Elias Allara ◽  
Olga Anufrieva ◽  
Pauli Ohukainen ◽  
...  
Keyword(s):  
Apolipoprotein B ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Triglyceride Composition ◽  
Cholesterol Concentration ◽  
Resonance Spectroscopy ◽  
Low Density ◽  
Triglyceride Content ◽  
Cetp Inhibition

AbstractBackgroundCETP inhibition reduces vascular event rates but confusion surrounds its low-density lipoprotein (LDL)-cholesterol effects. We sought to clarify associations of genetic inhibition of CETP on detailed lipoproteins.Methods and ResultsWe used variants associated withCETP(rs247617) andHMGCR(rs12916) expression in 62,400 Europeans with detailed lipoprotein profiling from nuclear magnetic resonance spectroscopy. Genetic associations were scaled to 10% lower risk of coronary heart disease (CHD). Associations of lipoprotein measures with risk of incident CHD in three population-based cohorts (770 cases) were examined.CETPandHMGCRhad near-identical associations with LDL-cholesterol concentration estimated by Friedewald-equation.HMGCRhad a relatively consistent effect on cholesterol concentrations across all apolipoprotein B-containing lipoproteins.CETPhad stronger effects on remnant and very-low-density lipoprotein cholesterol but no effect on cholesterol concentrations in LDL defined by particle size (diameter 18–26 nm) (-0.02SD 95%CI: -0.10, 0.05 forCETPversus -0.24SD, 95%CI -0.30, -0.18 forHMGCR).CETPhad profound effects on lipid compositions of lipoproteins, with strong reductions in the triglyceride content of all highdensity lipoprotein (HDL) particles. These alterations in triglyceride composition within HDL subclasses were observationally associated with risk of CHD, independently of total cholesterol and triglycerides (strongest HR per 1-SD higher triglyceride composition in very-large HDL 1.35; 95%CI: 1.18, 1.54).ConclusionCETP inhibition does not affect size-specific LDL cholesterol but may lower CHD risk by lowering cholesterol in other apolipoprotein-B containing lipoproteins and lowering triglyceride content of HDL particles. Conventional composite lipid assays may mask heterogeneous effects of lipid-altering therapies.

Lipoproteins during oral and cutaneous administration of oestradiol-17β to menopausal women

1982 ◽  
Vol 101 (4) ◽  
pp. 597-602 ◽  
Author(s):  
Lars Fåhraeus ◽  
Ulf Larsson-Cohn ◽  
Lars Wallentin
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Clinical Results ◽  
Point Of View ◽  
Clinical Effects ◽  
Low Density ◽  
Oestradiol Treatment ◽  
Menopausal Women ◽  
Post Menopausal ◽  
Cutaneous Administration

Abstract. Thirty-eight post-menopausal women were randomly allocated to substitution treatment with either oestradiol-17β orally (2–4 mg) or cutaneously (3 mg). The concentrations of cholesterol (C), triglycerides (TG) and phospholipids were determined in the high density lipoprotein (HDL)-, the low density lipoprotein (LDL)- and the very low density lipoprotein (VLDL)- fractions twice before medication and after 2, 4 and 6 months of treatment. Both treatments gave satisfactory clinical results. Oral doses increased the HDL and decreased the LDL thus raising the HDL-C/LDL-C ratio. The higher oral dose also increased the TG concentration. Cutaneous oestradiol gave only minimal changes of the lipoproteins. The lipoprotein changes observed during treatment with oral oestradiol might reduce the risk for atherosclerotic disease. Therefore, from a lipoprotein point of view, oral oestradiol treatment probably could be considered beneficial. The cutaneous oestradiol treatment had comparable clinical effects without any influence on the lipoprotein pattern.

Abstract 566: MicroRNA-146a Deficiency Prevents PCSK9 Gain-of-Function Mutation-induced Hypercholesterolemia in Mice

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Shayan Mohammadmoradi ◽  
Aida Javidan ◽  
Weihua Jiang ◽  
Jessica Moorleghen ◽  
Venkateswaran Subramanian
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Western Diet ◽  
Size Exclusion ◽  
Gel Chromatography ◽  
Low Density ◽  
Distribution Analysis ◽  
Gain Of Function ◽  
Ldl Particles

Background and Objective: Mimetic mediated activation of microRNA 146a (miR-146a) reduces atherosclerosis via suppression of nuclear factor-κB-driven inflammation in mice. The purpose of this study was to determine whether miR-146a influences plasma cholesterol in hypercholesterolemic mice. Methods and Results: To induce hypercholesterolemia, female C57BL/6 miR-146a WT (n=8) and miR-146a KO (n=8) mice were injected intraperitoneally with an adeno-associated viral vector (AAV) expressing the proprotein convertase subtilisin/kexin type 9 (PSCK9 D377Y) gain-of-function mutant at a dose of 3 x 10 10 genomic copies/mouse. After infection, mice were fed a Western diet (21% wt/wt milk fat; 0.15% wt/wt cholesterol) for sixteen weeks, and plasma PCSK9 and total cholesterol concentrations were monitored monthly using an enzymatic assay. Plasma PCSK9 concentrations were profoundly increased 4 weeks post injection (Baseline: WT - 179 ± 12 vs KO - 207 ± 12; Week 4: WT - 1700 ± 148 vs KO - 2689 ± 305 ng/ml) and remained significantly high during 16 weeks (WT - 882 ± 142 vs KO - 718 ± 109 ng/ml; p<0.05 vs baseline) of Western diet feeding. Consistent with increased plasma PCSK9 concentrations, plasma cholesterol concentrations were increased in both groups of mice. Interestingly, miR-146a KO group mice showed less significant increase in plasma cholesterol compared to WT group (Baseline: WT - 88 ± 3 vs KO - 83 ± 3; Week 4: WT - 328 ± 25 vs KO - 195 ± 18 mg/dl) irrespective of the comparable plasma PCSK9 concentrations. Also, lipoprotein distribution analysis with size exclusion gel chromatography revealed that miR-146a KO mice showed a strong reduction in high density lipoprotein (HDL) particles while very low density lipoprotein (VLDL) and low density lipoprotein (LDL) particles were not affected. Conclusion: Our findings suggests that miR146a plays a critical role in the regulation of HDL particles in PCSK9 gain-of-function mutant-induced hypercholesterolemia in mice. Future studies will identify gene targets influenced by miR-146a in regulating HDL-cholesterol in hypercholesterolemic mice.

Lipoprotein cholesterol concentrations in the plasma of human subjects as measured in the fed and fasted states.

1988 ◽  
Vol 34 (12) ◽  
pp. 2456-2459 ◽  
Author(s):  
J S Cohn ◽  
J R McNamara ◽  
E J Schaefer
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Triglyceride ◽  
Lipoprotein Cholesterol ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Plasma Triglyceride Concentration ◽  
Triglyceride Concentration ◽  
Friedewald Formula

Abstract Lipoprotein cholesterol concentrations in plasma are routinely estimated by using the Friedewald formula, whereby very-low-density lipoprotein cholesterol (VLDL-C) is estimated to be one-fifth the plasma triglyceride concentration. Ordinarily, this formula is applied only to plasma sampled from patients in the fasted state. To determine whether lipoprotein cholesterol measurements are altered substantially in plasma sampled from nonfasting subjects, we obtained postprandial blood samples from 22 healthy subjects (nine men, 13 women, ages 22-79 years) fed a fat-rich meal (1 g fat per kilogram body wt.). The plasma triglyceride concentration increased postprandially in all subjects (233 +/- 16% of baseline at 3 h). The mean cholesterol concentration in plasma was essentially unchanged. High-density lipoprotein cholesterol (HDL-C) was significantly decreased (94 +/- 2% at 3 h, P less than 0.001). VLDL-C and low-density lipoprotein cholesterol (LDL-C), estimated by the Friedewald formula, were compared with measurements obtained by modified Lipid Research Clinics (LRC) methodology. As measured by either method, VLDL-C increased and LDL-C decreased significantly after the fat-rich meal. These postprandial changes were significantly greater (P less than 0.01) when estimated by the Friedewald formula than by LRC methodology. We conclude that (a) lipoprotein cholesterol concentrations measured in the fed subject differ significantly from those measured in the fasted subject, and (b) plasma must be obtained after at least a 12-h fast if an individual's risk of coronary heart disease is to be accurately assessed.

Enhanced Hepatic Uptake of Low Density Lipoprotein by Lovastatin (Mevinolin) in Man

1990 ◽  
Vol 2 (S2) ◽  
pp. 37-39 ◽  
Author(s):  
Markku J. Savolainen ◽  
Kari Kervinen ◽  
Juhani Heikkilä ◽  
Antero Kesäniemi
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hepatic Uptake ◽  
Low Density
Sign in / Sign up

Export Citation Format

Share Document