ubiquinone and Hypertriglyceridemia

ubiquinone has been researched along with Hypertriglyceridemia* in 3 studies

Trials

2 trial(s) available for ubiquinone and Hypertriglyceridemia

ArticleYear
Possible role of ubiquinone in the treatment of massive hypertriglyceridemia resistant to PUFA and fibrates.
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2005, Volume: 59, Issue:6

    To describe the effect of Coenzyme Q10 (CoQ10) (added to either a fibrate, or polyunsaturated fatty acids (PUFA) or association of both) in patients affected by massive hypertriglyceridemia (MHTG) resistant to fibrates and PUFA.. Open, sequential, comparative intervention study.. Specialised centres for dyslipidemia management.. Fifteen subjects (mean age: 45.1+/-12.5 years) affected by MHTG and hyporesponsive to either fibrates, or PUFA, or fibrates-PUFA association, and 15 age-matched subjects regularly responders to PUFA and fenofibrate treatment.. Treatment for periods of 6 weeks each with the following consecutive treatments: CoQ10 150 mg/day, PUFA 3000 mg/day, fenofibrate 200 mg/day, PUFA 3000 mg/day+fenofibrate 200 mg/day, PUFA 3000 mg/day+CoQ10 150 mg/day, fenofibrate 200 mg/day+CoQ10 150 mg/day, and finally, fenofibrate 200 mg/day+PUFA 3000 mg/day + CoQ10 150 mg/day.. CoQ10 supplementation did not improve any monitored parameter in the control group except for systolic and diastolic blood pressure, creatinine and Lp(a) plasma levels, both during fenofibrate and/or PUFA treatment. In MHTG group, CoQ10 supplementation significantly improved TG, TC, Lp(a), uric acid and blood pressure during fenofibrate treatment, but only Lp(a) and blood pressure during PUFA treatment. Fenofibrate appeared to have better effect on hsCRP and gamma-GT plasma levels than PUFA. No significant change was observed in any group and under any treatment in regards to homocysteinemia, PAI-1, or t-PA.. Even though the mechanism of action through which the effects were obtained is yet to be elucidated, adding CoQ10 to fenofibrate could improve the drug's efficacy in MHTG patients not responding to fenofibrate alone.

    Topics: Adult; Blood Pressure; Cholesterol; Coenzymes; Creatinine; Drug Resistance; Drug Therapy, Combination; Fatty Acids, Unsaturated; Female; Fenofibrate; gamma-Glutamyltransferase; Humans; Hypertriglyceridemia; Lipoprotein(a); Male; Middle Aged; Time Factors; Treatment Outcome; Triglycerides; Ubiquinone; Uric Acid

2005
Monounsaturated diet lowers LDL oxidisability in type IIb and type IV dyslipidemia without affecting coenzyme Q10 and vitamin E contents.
    BioFactors (Oxford, England), 1999, Volume: 9, Issue:2-4

    The purpose of the present study was to evaluate the effects of MUFA vs PUFA enriched diets on the plasma and LDL lipid profile and antioxidant contents in mild hypercholesterolemic and triglyceridemic subjects. The study was divided in two consecutive diet periods. Two groups of 11 dyslipidemic patients each (type IIb and type IV) were recruited and during the first period (lasting four weeks) received a linoleic rich diet while during the following four weeks took an oleate rich diet. Both groups showed no significant changes in cholesterol and TG concentration either in plasma or in LDL. Coenzyme Q10 and vitamin E were also unaffected by the dietary treatments. LDL proneness to be oxidatively modified increased after dietary PUFA administration and markedly decreased following the virgin olive oil enriched diet. In fact, LDL from hypertrigliceridemic subjects on a oleate-enriched diet displayed a 26% (p < 0.05) longer lag-phase in conjugated dienes generation than during linoleate-enriched diet and at recruitment. In hypercholesterolemic subjects similar results were obtained: the lag-phase was 28% longer after MUFA diet that after PUFA diet. No differences were found in the maximum propagation rate and maximum concentration of conjugated dienes among dietary periods and at recruitment. Since we found that the vit. E and CoQ10 levels in plasma and in LDL particles remained unchanged during the course of the study, we may conclude that LDL proneness to undergo oxidative modifications is mainly the result of compositional change due to the enrichment from the different diets of the relative fats.

    Topics: Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Coenzymes; Dietary Fats, Unsaturated; Fatty Acids, Monounsaturated; Fatty Acids, Unsaturated; Humans; Hypercholesterolemia; Hypertriglyceridemia; Olive Oil; Plant Oils; Soybean Oil; Triglycerides; Ubiquinone; Vitamin E

1999

Other Studies

1 other study(ies) available for ubiquinone and Hypertriglyceridemia

ArticleYear
Treatment of massive hypertriglyceridemia resistant to PUFA and fibrates: a possible role for the coenzyme Q10?
    BioFactors (Oxford, England), 2005, Volume: 23, Issue:1

    To describe the effect of CoQ10 (added to either a fibrate, or PUFA or association of both) in patients affected by massive hypertriglyceridemia (MHTG) resistant to fibrates and PUFA.. Open, sequential, comparative intervention study.. Specialised centres for dyslipidemia management.. 15 subjects (mean age: 45.1 +/- 12.5 years) affected by MHTG and hyporesponsive to either fibrates, or PUFA, or fibrates-PUFA association, and 15 age-matched subjects regularly responders to PUFA and fenofibrate treatment.. Treatment for periods of 6 weeks each with the following consecutive treatments: CoQ10 150 mg/day, PUFA 3000 mg/day, fenofibrate 200 mg/day, PUFA 3000 mg/day + fenofibrate 200 mg/day, PUFA 3000 mg/day + CoQ10 150 mg/day, fenofibrate 200 mg/day + CoQ10 150 mg/day, and finally, fenofibrate 200 mg/day + PUFA 3000 mg/day + CoQ10 150 mg/day.. CoQ10 supplementation improved, in the control group, systolic and diastolic blood pressure, creatinine and Lp(a) plasma levels, both during fenofibrate and/or PUFA treatment. In MHTG group, CoQ10 supplementation significantly improved TG, TC, Lp(a), uric acid and blood pressure during fenofibrate treatment, but only Lp(a) and blood pressure during PUFA treatment. Fenofibrate appeared to have better effect on hsCRP and gamma-GT plasma levels than PUFA. No significant change was observed in any group and under any treatment in regards to homocysteinemia, PAI-1, or t-PA.. Even though the mechanism of action through which the effects were obtained is yet to be elucidated, adding CoQ10 to fenofibrate could improve the drug's efficacy in MHTG patients not responding to fenofibrate alone.

    Topics: Adult; Blood Pressure; Cholesterol; Coenzymes; Creatinine; Diet; Drug Resistance; Fatty Acids, Omega-3; Female; Fenofibrate; gamma-Glutamyltransferase; Humans; Hypertriglyceridemia; Lipoprotein(a); Male; Middle Aged; Triglycerides; Ubiquinone; Uric Acid

2005