Coenzyme Q10 Improves Endothelial Dysfunction in Statin-Treated Type 2 Diabetic Patients
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作者:
Hamilton, Sandra J.
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Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, Australia
Hamilton, Sandra J.
[1
]
Chew, Gerard T.
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Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, Australia
Chew, Gerard T.
[1
]
Watts, Gerald F.
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Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, Australia
Watts, Gerald F.
[1
]
机构:
[1] Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6009, Australia
OBJECTIVE - The vascular benefits of statins might be attenuated by inhibition of coenzyme Q(10) (CoQ(10)) synthesis. We investigated whether oral CoQ(10) supplementation improves endothelial dysfunction in statin-treated type 2 diabetic patients. RESEARCH DESIGN AND METHODS - in a double-blind crossover study, 23 statin-treated type 2 diabetic patients With LDL cholesterol <2.5mmol/l and endothelial dysfunction (brachial artery How-mediated dilatation [FMD] <5.5%) were randomized to oral CoQ(10) (200 mg/day) or placebo for 12 weeks. We measured brachial artery FMD and nitrate-mediated dilatation (NMD) by ultrasonography. Plasma F-2-isoprostane and 24-h urinary 20-hydroxyeicosatetraenoic acid (HETE) levels were measured as systemic oxidative stress markers. RESULTS - Compared with placebo, CoQ(10) supplementation increased brachial artery FMD by 1.0 +/- 0.5% (P = 0.04), but did not alter NMD (P = 0.66). CoQ(10) supplementation also did not alter plasma F.-isoprostane (P = 0.58) or urinary 20-HETE levels (P = 0.28). CONCLUSIONS - CoQ(10)) supplementation improved endothelial dysfunction in statin-treated type 2 diabetic patients, possibly by altering local vascular oxidative stress.
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Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, Australia
Chew, GT
;
Watts, GF
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Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, Australia
机构:
Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, Australia
Chew, GT
;
Watts, GF
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h-index: 0
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Univ Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, AustraliaUniv Western Australia, Royal Perth Hosp Unit, Sch Med & Pharmacol, Perth, WA 6847, Australia