Short-term effects of β-adrenoceptor blocking drugs with and without cardioselectivity and intrinsic sympathomimetic activity on lipoprotein metabolism in hypertriglyceridaemic patients and in normal men

1985 ◽  
Vol 69 (6) ◽  
pp. 713-719 ◽  
Author(s):  
P. N. Durrington ◽  
W. C. Brownlee ◽  
D. M. Large
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Cholesterol Concentration ◽  
Intrinsic Sympathomimetic Activity ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Serum Triglycerides ◽  
Β Blocker ◽  
Normal Men

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.

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.

Elevation of Low-Density Lipoprotein Cholesterol Concentration with Over-the-Counter Fish Oil Supplementation

2007 ◽  
Vol 41 (7-8) ◽  
pp. 1296-1300 ◽  
Author(s):  
Jennifer M Malinowski ◽  
Kimberly Metka
Keyword(s):  
Fish Oil ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Over The Counter ◽  
Epa And Dha ◽  
Fish Oil Supplementation

Objective: To report a case of elevated low-density lipoprotein cholesterol (LDL-C) concentration in a patient taking fish oil supplements for hypertriglyceridemia. Case Summary: A 63-year-old white woman had been taking 2.7 g of eico-sapentaenotc acid (EPA) and docosahexaenoic acid (DHA) daily in 9 g of over-the-counter (OTC) fish oil capsules for triglyceride lowering. Prior to the adverse event, she had baseline fasting triglyceride (TG) and LDL-C concentrations of 278 mg/dL and 106 mg/dL, respectively. After 6 weeks of treatment with fish oil, fasting TG levels decreased by 47.5% (-132 mg/dL) and the LDL-C increased by 75% (+80 mg/dL). Discontinuation of therapy for 6 weeks resulted in TG returning to high concentrations (334 mg/dL; +56 mg/dL change from baseline) and LDL-C decreasing toward baseline (143 mg/dL; +37 mg/dL change from baseline). Discussion: Fish oil, an omega-3 polyunsaturated fatty acid, consists of EPA and DHA. EPA and DHA are thought to inhibit the synthesis of triglycerides in the liver. Type IV dyslipidemic patients may develop increased LDL-C levels while taking fish oil to lower triglycerides due to possible down-regulation of the LDL-C receptor in hepatic cells and formation of larger LDL particles. Use of the Naranjo probability scale indicates a probable relationship between elevations in LDL-C from baseline and initiation of fish oil treatment for hypertriglyceridemia. It is unknown whether any component within this particular product could have contributed to such an unusual elevation in LDL-C. Conclusions: This case documents a much higher LDL-C elevation associated with OTC fish oil supplementation than has been previously identified in the literature. Healthcare providers should be advised that LDL-C levels may increase with use of OTC fish oil and should monitor patients periodically for such elevations. The significance of this Increase on clinical outcomes is not known.

scholarly journals Rutin ameliorates carbon tetrachloride (CCl4)-induced hepatorenal toxicity and hypogonadism in male rats

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7011 ◽  
Author(s):  
Hany Elsawy ◽  
Gehan M. Badr ◽  
Azza Sedky ◽  
Basem M. Abdallah ◽  
Abdullah M. Alzahrani ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Sperm Quality ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Testosterone ◽  
Lipoprotein Cholesterol ◽  
Male Rats ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Serum Triglycerides

Rutin, a food derived-polyphenolic bioflavonoid, has been acknowledged for several health benefits. This study aims to explore the ameliorative effects of rutin against carbon tetrachloride (CCl4) toxicity in male rats. Adult male rats were given either CCl4 (30% in olive oil, 3 ml/kg b.w. intraperitoneally) alone or in combination with rutin (70 mg/kg intragastrically) twice a week for 4 weeks. Our data showed that rutin mitigated CCl4 hepatorenal damage, as indicated by diagnostic markers (i.e., transaminases, alkaline phosphatase, total bilirubin, total protein, albumin, urea, uric acid and creatinine), and histopathological findings. In addition, CCl4 induced profound elevation of free radical generation and oxidative stress, as evidenced by increasing lipid peroxidation and reducing catalase, superoxide dismutase and glutathione peroxidase activities in liver, kidney and testicular tissues; these effects were suppressed by coexposure with rutin. Moreover, the increase in the levels of serum triglycerides, cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol induced by CCl4 was effectively counteracted by rutin. The decrease in the level of high-density lipoprotein cholesterol in the CCl4 group was also counteracted by rutin treatment. Interestingly, the decreased levels of hormonal mediators associated with sperm production, including serum testosterone, luteinizing hormone and follicle-stimulating hormone, and the impaired sperm quality induced by CCl4 were reversed by rutin. Data from the current study clearly demonstrated that rutin supplementation could at least partly overcome CCl4-induced hepatotoxicity, nephrotoxicity and reproductive toxicity by antioxidant and antidyslipidemic effects.

Five methods for determining low-density lipoprotein cholesterol compared.

1984 ◽  
Vol 30 (11) ◽  
pp. 1797-1800 ◽  
Author(s):  
P N Demacker ◽  
A G Hijmans ◽  
B J Brenninkmeijer ◽  
A P Jansen ◽  
A van 't Laar
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Very Low Density Lipoproteins ◽  
Serum Triglycerides ◽  
Type Iii ◽  
Friedewald Formula

Abstract We evaluated three precipitation methods for determination of low-density lipoprotein cholesterol in serum and an indirect method involving the Friedewald formula (Clin Chem 18: 499-502, 1972) by comparison with results by ultracentrifugation. The results of all methods for 83 sera, including 59 hyperlipidemic type IIA, IIB, and IV sera agreed very well, at least for concentrations of serum triglycerides below 8 mmol/L. The accuracy of the Friedewald formula was confirmed in 285 other sera, including 66 sera with triglycerides content between 4.52 and 8.0 mmol/L. For type III sera, the precipitation methods produced similar values to those obtained with the Friedewald formula, all being much higher than the ultracentrifugation values. Density-gradient ultracentrifugation showed that the very-low-density lipoprotein remnants in type III sera almost completely coprecipitated with the low-density lipoproteins. The precipitation methods are not only accurate but also very precise (CV less than 5%); they can therefore be used in clinical laboratories to measure atherogenic low-density lipoproteins plus the remnants of very-low-density lipoproteins. However, when serum triglycerides and high-density lipoprotein cholesterol also are determined, the Friedewald formula is a reliable alternative.

Small dense low-density lipoprotein cholesterol concentration and carotid atherosclerosis

2009 ◽  
Vol 202 (2) ◽  
pp. 582-588 ◽  
Author(s):  
Tetsuo Shoji ◽  
Sawako Hatsuda ◽  
Shoko Tsuchikura ◽  
Kayo Shinohara ◽  
Eiji Kimoto ◽  
...  
Keyword(s):  
Carotid Atherosclerosis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol

β-Receptor-Blocking Agents May Reverse or Prevent Diuretic-Induced Increases in Serum Low-Density Lipoprotein Cholesterol

1981 ◽  
Vol 61 (s7) ◽  
pp. 437s-439s ◽  
Author(s):  
A. Meier ◽  
H. Schiffl ◽  
P. Weidmann ◽  
R. Mordasini ◽  
W. Riesen ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Group I ◽  
Β Blocker ◽  
Β Receptor

1. The effect of treatment with a thiazide-like diuretic alone or combined with a β-adrenoceptor blocker on serum lipoproteins was investigated in 35 patients with essential hypertension. 2. In group I (18 patients), serum low-density lipoprotein cholesterol was increased (P < 0.001) during monotherapy with chlorthalidone (100 mg/day) but not during combined chlorthalidone-β-blocker therapy. 3. This tendency was similar in subgroups studied with an inverse sequence of drug administration. In subgroup IA (11 men), a 22% increase (P < 0.01) in low-density lipoprotein cholesterol after 6 weeks of chlorthalidone was reversed after use of a β-blocker as well as chlorthalidone; in subgroup IB (five men, two post-menopausal women), low-density lipoprotein cholesterol was increased by 41% (P < 0.05) above placebo values 6 weeks after withdrawal of the β-blocker from combination therapy. 4. In group II (18 men), low-density lipoprotein cholesterol was increased by 13% (P < 0.025) after 4 weeks of monotherapy with clopamide (5 mg/day) but restored to control levels 4 weeks after addition of pindolol (10 mg/day). 5. No significant changes occurred during any treatment phase in high-density lipoprotein cholesterol. 6. Certain β-receptor blocking agents may prevent or reverse diuretic-induced increases in serum low-density lipoprotein cholesterol.

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