Effect of Phenobarbitone on Plasma Apolipoprotein B and Plasma High-Density-Lipoprotein Cholesterol in Normal Subjects

1979 ◽  
Vol 56 (5) ◽  
pp. 501-504 ◽  
Author(s):  
P. N. Durrington

1. Further observations from an earlier study in which phenobarbitone in a dose of 180 mg daily was administered to ten normal men and women for 3 weeks are reported. There was a significant increase in plasma high-denity-lipoprotein (HDL) cholesterol concentration and in the concentration of both total plasma and low-density-lipoprotein (LDL) apolipoprotein B. 2. There was no change in the ratios of the cholesterol: apolipoprotein B and triglyceride: apolipoprotein B in LDL. 3. There was no significant change in plasma very-low-density-lipoprotein (VLDL) apolipoprotein B concentration and the proportion of lipid and apolipoprotein B in VLDL remained unchanged. 4. There was no change in the ratio of HDL:LDL cholesterol concentrations.

1986 ◽  
Vol 55 (02) ◽  
pp. 173-177 ◽  
Author(s):  
K Desai ◽  
J S Owen ◽  
D T Wilson ◽  
R A Hutton

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.


2018 ◽  
Author(s):  
Johannes Kettunen ◽  
Michael V. Holmes ◽  
Elias Allara ◽  
Olga Anufrieva ◽  
Pauli Ohukainen ◽  
...  

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.


1992 ◽  
Vol 82 (6) ◽  
pp. 701-708 ◽  
Author(s):  
G. L. Warwick ◽  
C. J. Packard ◽  
L. Murray ◽  
D. Grierson ◽  
J. P. Stewart ◽  
...  

1. The effect of inhibiting the rate-limiting enzyme (3-hydroxy-3-methylglutaryl-CoA reductase, EC 1.1.1.88) in cholesterol synthesis on plasma lipid and lipoprotein concentrations was investigated in 16 patients with primary glomerular disease, heavy proteinuria, well-preserved renal function and hypercholesterolaemia. 2. Detailed studies of low-density lipoprotein metabolism were performed on eight patients before and after 12 weeks of simvastatin therapy. Radioiodinated tracers were used to quantify the fractional catabolic rate of low-density lipoprotein by apolipoprotein B/E receptors and alternative pathways. 3. Simvastatin produced consistent reductions in total plasma cholesterol concentration (median 36.9%), plasma low-density lipoprotein-cholesterol concentration (43.6%) and apolipoprotein B pool size (29.9%). 4. In contrast, the changes in kinetic parameters of low-density lipoprotein metabolism showed no clear pattern. Although an increase in the receptor-mediated catabolism of low-density lipoprotein was demonstrated in five patients, no change or a slight decrease was seen in three patients. Production rates were not significantly altered, although there was a slight decrease in the median value (from 12.4 to 9.7 mg day−1 kg−1). Plasma lathosterol concentration was reduced in all eight patients (range 34–71%), indirectly confirming significant inhibition of cholesterol synthesis. 5. These results suggest that, as in patients with primary moderate hyperlipidaemia, the significant cholesterol-lowering effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in the nephrotic syndrome is accompanied by variable changes in lipoprotein metabolism. The reasons for this heterogeneous response are unclear. This reflects our limited understanding of the metabolic basis of nephrotic hyperlipidaemia and the relationship between hepatic sterol synthesis and plasma lipoprotein kinetics.


2005 ◽  
Vol 75 (3) ◽  
pp. 211-217 ◽  
Author(s):  
Schlegelmilch ◽  
Brandsch ◽  
Stangl ◽  
Eder

Two experiments were conducted to determine whether molasses might exert effects on serum lipoproteins. In experiment 1, 24 rats were divided into two groups and fed diets containing liquid molasses from sugar beet or sucrose (7.71 g of molasses dry matter or sucrose per kg of diet). The second experiment included four groups of rats (n = 12/group) and was conducted in a bifactorial design, with the factors being molasses (non-supplementation vs. supplementation of 77.1 g of molasses dry matter per kg of diet at the expense of sucrose) and dietary cholesterol (0 vs. 5 g/kg diet). In experiment 1, the ratio of low-density lipoprotein (LDL) to high-density lipoprotein (HDL) cholesterol concentration tended to be lower in rats fed the molasses diet than in rats fed the control diet (p < 0.15). In experiment 2, rats fed the molasses diet had higher concentrations of HDL cholesterol (+ 26%) than control rats fed diets without molasses (p < 0.05). This effect was independent of the dietary cholesterol concentration. Concentrations of cholesterol in LDL, very low-density lipoprotein (VLDL), and liver as well as concentrations of triacylglycerols in plasma and liver remained unaffected by molasses in both experiments. In conclusion, the results of this study suggest that supplementation of molasses is effective at raising HDL cholesterol levels in rats.


2020 ◽  
Author(s):  
X Wang ◽  
Di Zhu ◽  
Yang Du ◽  
Yangbo Sun ◽  
Linda Snetselaar

Abstract Background: The control of blood glucose and athero­genic cholesterol particle concentrations is fundamental for patients with diabetes. The objective of this study was to examine trends in levels of apolipoprotein B (apo B), non-high-density lipoprotein (non-HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and hemoglobin A1c (A1C) and changes in the proportion of patients who achieved their glycemic and lipid goals between 2005 and 2018.Methods: We conducted a serial cross-sectional analysis of the US nationally representative data from the National Health and Nutrition Examination Surveys form 2005 through 2018. Results: In total, 5536 adults aged 20 years or older with diabetes were included (weighted mean age, 60.2 years; female, 50.1%). Among all adults with diabetes, the age-adjusted mean apo B levels did not decrease significantly from 2005 to 2016 (P =0.077). The age-adjusted mean non-HDL cholesterol levels reduced significantly (P =0.004) from 2005 to 2018. In 2017-2018, 55.3% of patients achieved the A1C goal of <7% and 43.8% achieved the non-HDL cholesterol goal of <130 mg/dl. In 2015-2016, 47.3% achieved the apo B goal of <90 mg/dL, 57.2% achieved the LDL cholesterol goal of <100 mg/dl, while 30.6% achieved all four glycemic and lipid goals. The success rates for achieving the goals of apo B, non-HDL cholesterol, and LDL cholesterol were higher in older compared with younger subjects, while white patients exhibited better glycemic control than Mexican Americans and non-Hispanic black patients.Conclusion: Among adults with diabetes, there was a significant reduction in non-HDL cholesterol level while there was no change in levels of apo B, LDL cholesterol or A1C over the past decade. Nevertheless, large percentages of adults with diabetes continue to have higher levels of apo B, non-HDL cholesterol, LDL cholesterol, and A1C.


1985 ◽  
Vol 69 (6) ◽  
pp. 713-719 ◽  
Author(s):  
P. N. Durrington ◽  
W. C. Brownlee ◽  
D. M. Large

1. In six patients with hypertriglyceridaemia presenting whilst receiving treatment with β-adrenoreceptor blocking drugs (mean serum triglycerides 31.2 mmol/l) the half-life (t1/2) of an intravenously administered triglyceride emulsion was 32.8 ± 7.9 min (mean ± sem) on β-blocker and 22.8 ± 4.8 min after stopping β-blocker treatment. 2. In three of these patients subsequent administration of a β-blocker with intrinsic sympathomimetic activity had no effect on t1/2. 3. In a cross-over trial of placebo, atenolol (β1-blocker), propranolol (β1- and β2-blocker) and pindolol (β1- and β2-blocker with intrinsic sympathomimetic activity) in 11 normal men t1/2 was 11.8±0.9, 12.6±1.1, 14.3±1.7 and 12.4±1.1 min respectively. None of the apparent differences achieved statistical significance, but in two men marked increases in t1/2 occurred on propranolol. 4. The concentrations of serum triglycerides and very low density lipoprotein cholesterol in the normal men were, however, increased by β-blockade, most markedly by pindolol. 5. Serum high density lipoprotein (HDL) cholesterol concentration decreased in normal men on β-blockers, most clearly on atenolol and propranolol. This decrease was due to a reduction in cholesterol in the HDL2 subfraction. 6. No statistically significant effects on serum low density lipoprotein cholesterol or apolipoprotein B concentrations occurred in the normal men. 7. The doses of atenolol and propranolol used in this study were equipotent as judged by the heart rate response to exercise.


1993 ◽  
Vol 85 (3) ◽  
pp. 269-275 ◽  
Author(s):  
Robert A. Hegele ◽  
George Zahariadis ◽  
Alexandra L. Jenkins ◽  
Philip W. Connelly ◽  
Hanoch Kashtan ◽  
...  

1. We hypothesized that differences within genes whose protein products are involved in apolipoprotein B metabolism could influence the response of plasma apolipoprotein B-containing lipoprotein concentrations to increases in dietary fibre. 2. We studied 67 subjects (43 men and 24 women) who had taken part in parallel 2 week metabolic dietary studies involving either wheat bran or oat bran supplementation. Fasting blood lipid, lipoprotein and apolipoprotein concentrations were measured at the start and end of the 2 week metabolic period. Genotypes were determined using DNA markers for the low-density lipoprotein receptor, apolipoprotein B, apolipoprotein CIII and hepatic lipase gene loci. 3. Reductions in plasma concentrations of apolipoprotein B were significantly different depending on genotype determined with a low-density lipoprotein receptor DNA marker (P = 0.03). There was no significant variation in the reduction of plasma total cholesterol, low-density lipoprotein cholesterol or apolipoprotein B concentrations for alleles of other genes tested. 4. Thus, genetic variability is associated with inter-individual differences in the fibre-related reduction in plasma apolipoprotein B and apolipoprotein B-containing lipoprotein concentrations. Implementation of current dietary recommendations to reduce plasma lipoprotein levels with fibre may have variable effects in different individuals in part because of structural differences in candidate genes whose products are involved in lipoprotein metabolism.


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