Effects of coenzyme Q10 supplementation on inflammatory markers (high-sensitivity C-reactive protein, interleukin-6, and homocysteine) in patients with coronary …

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DOI: 10.1016/j.nut.2011.11.008 · Source: PubMed
Abstract
The purpose of this study was to investigate the effects of coenzyme Q10 supplementation on inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], interleukin-6 [IL-6], and homocysteine) in patients with coronary artery disease (CAD). Patients with CAD (n = 51) were randomly assigned to a placebo group (n = 14) or one of two coenzyme Q10-supplemented groups (60 mg/d, Q10-60 group, n = 19; 150 mg/d, Q10-150 group, n = 18). The intervention was administered for 12 wk. Plasma coenzyme Q10 concentration, inflammatory markers (hs-CRP, IL-6, and homocysteine), malondialdehyde, and superoxide dismutase activities were measured. Forty subjects with CAD completed the intervention study. The plasma coenzyme Q10 concentration increased significantly in the Q10-60 and Q10-150 groups (P < 0.01). After 12 wk of intervention, the inflammatory marker IL-6 (P = 0.03) was decreased significantly in the Q10-150 group. Subjects in the Q10-150 group had significantly lower malondialdehyde levels and those in the Q10-60 (P = 0.05) and Q10-150 (P = 0.06) groups had greater superoxide dismutase activities. Plasma coenzyme Q10 was inversely correlated with hs-CRP (r = -0.20, P = 0.07) and IL-6 (r = -0.25, P = 0.03) at baseline. After supplementation, plasma coenzyme Q10 was significantly correlated with malondialdehyde (r = -0.35, P < 0.01) and superoxide dismutase activities (r = 0.52, P < 0.01). However, there was no correlation between coenzyme Q10 and homocysteine. Coenzyme Q10 supplementation at a dosage of 150 mg appears to decrease the inflammatory marker IL-6 in patients with CAD.
Applied nutritional investigation
Effects of coenzyme Q10 supplementation on inammatory markers
(high-sensitivity C-reactive protein, interleukin-6, and homocysteine)
in patients with coronary artery disease
Bor-Jen Lee M.D.
a
,
b
, Yi-Chia Huang Ph.D.
a
,
c
, Shu-Ju Chen Ph.D.
d
, Ping-Ting Lin Ph.D.
a
,
c
,
*
a
School of Nutrition, Chung Shan Medical University, Taichung, Taiwan
b
Intensive Care Unit, Taichung Veterans General Hospital, Taichung, Taiwan
c
Department of Nutrition, Chung Shan Medical University Hospital, Taichung, Taiwan
d
Department of Nutrition and Health Science, Chung Chou University of Science and Technology, Changhua, Taiwan
article info
Article history:
Received 15 April 2011
Accepted 9 November 2011
Keywords:
Coenzyme Q10
Inammation
High-sensitivity C-reactive protein
Interleukin-6
Coronary artery disease
Antioxidant
abstract
Objective: The purpose of this study was to investigate the effects of coenzyme Q10 supplemen-
tation on inammatory markers (high-sensitivity C-reactive protein [hs-CRP], interleukin-6 [IL-6],
and homocysteine) in patients with coronary artery disease (CAD).
Methods: Patients with CAD (n ¼ 51) were randomly assigned to a placebo group (n ¼ 14) or one of
two coenzyme Q10-supplemented groups (60 mg/d, Q10-60 group, n ¼ 19; 150 mg/d, Q10-150
group, n ¼ 18). The intervention was administered for 12 wk. Plasm a coenzyme Q10 concentra-
tion, inammatory markers (hs-CRP, IL-6, and homocysteine), malondialdehyde, and superoxide
dismutase activities were measured.
Results: Forty subjects with CAD completed the intervention study. The plasma coenzyme Q10
concentration increased signicantly in the Q10-60 and Q10-150 groups (P < 0.01). After 12 wk of
intervention, the inammatory marker IL-6 (P ¼ 0.03) was decreased signicantly in the Q10-150
group. Subjects in the Q10-150 group had signicantly lower malondialdehyde levels and those in
the Q10-60 (P ¼ 0.05) and Q10-150 (P ¼ 0.06) groups had greater superoxide dismutase activities.
Plasma coenzyme Q10 was inversely correlated with hs-CRP (r ¼0.20, P ¼ 0.07) and IL-6 (r ¼0.25,
P ¼ 0.03) at baseline. After supplementation, plasma coenzyme Q10 was signicantly correlated with
malondialdehyde (r ¼0.35, P < 0.01) and superoxide dismutase activities (r ¼ 0.52, P < 0.01).
However, there was no correlation between coenzyme Q10 and homocysteine.
Conclusion: Coenzyme Q10 supplementation at a dosage of 150 mg appears to decrease the
inammatory marker IL-6 in patients with CAD.
Ó 2012 Elsevier Inc. All rights reserved.
Introduction
Coenzyme Q10 (also called ubiquinone) is a lipid-soluble
benzoquinone with 10 isoprenyl units in the side chain and is
a key component of the mitochondrial respiratory chain for
adenosine triphosphate synthesis [1,2]. Tissues with high-energy
requirements, such as the heart, kidney, liver, and skeletal
muscle cells, need a larger amount of coenzyme Q10 to synthe-
size adenosine triphosphate. Coenzyme Q10 is recognized as an
intracellular antioxidant that protects membrane phospholipids,
mitochondrial membrane protein, and low-density lipoprotein
against free radical-induced oxidative damage [3,4]. Coenzyme
Q10 can be synthesized in the tissue from farnesyl diphosphate
and tyrosine and can be obtained from the diet in an oxidized
form of which 75% to 95% is then converted into a reduced form
in the body; however, the total absorption of coenzyme Q10 is
thought to be less than 10% [5,6].
Cardiovascular disease is the leading cause of death world-
wide [7]. There is mounting evidence that in ammation plays
a role in the development of cardiovascular disease. In clinical
studies, the levels of homocysteine and high-sensitivity C-reac-
tive protein (hs-CRP) have commonly been used as inammatory
markers that contribute to the earlier stages of coronary artery
disease (CAD) [8,9]. Interleukin-6 (IL-6) is a messenger cytokine
This study was supported by grant NSC 97-2320-B-040-034-MY2 from the
National Science Council, Taiwan.
*
Corresponding author. Tel.: þ886-4-2473-0022, ext. 12187; fax: þ886-4-
2324-8175.
E-mail address: apt810@csmu.edu.tw (P.-T. Lin).
0899-9007/$ - see front matter Ó 2012 Elsevier Inc. All rights reserved.
doi:10.1016/j.nut.2011.11.008
Contents lists available at ScienceDirect
Nutrition
journal homepage: www.nutritionjrnl.com
Nutrition 28 (2012) 767772
that induces hepatic CRP production [10]. The relation between
coenzyme Q10 and inammation has been reported in cell [11,12]
and animal [13,14] models. In recent studies [15,16], however,
coenzyme Q10 supplementation has been found to have inu-
ence on inammatory markers in subjects with multiple
cardiovascular disease risk factors or in healthy subjects. To date,
fewer clinical studies have investigated the relation between
coenzyme Q10 and inammation in patients with CAD. As
a result, in this study, we investigated the effect of coenzyme Q10
supplementation (60 and 150 mg/d) on inammatory markers
(hs-CRP, IL-6, and homocysteine) in patients with CAD.
Materials and methods
Subjects
This study was designed as a randomized, parallel, placebo-controlled study.
Patients with CAD were recruited from the cardiology clinic of Taichung Veterans
General Hospital, which is a teaching hospital in central Taiwan. Patients iden-
tied as having at least 50% stenosis of one major coronary artery by cardiac
catheterization or underwent percutaneous transluminal coronary angioplasty
were enrolled in this study. Subjects with diabetes or liver or renal diseases were
excluded to minimize the inuence of other cardiovascular risk factors. Patients
under statin therapy or currently taking vitamin supplements were also
excluded. None of the subjects had developed acute myocardial infarction within
the previous 6 mo. Informed consent was obtained from each subject. This study
was approved by the institutional review board of Taichung Veterans General
Hospital.
Study protocol
With a sample size calculation, we expected that the change in the level of
hs-CRP would be 0.1 0.1 mg/dL after the coenzyme Q10 intervention; hence, the
desired power was set at 0.8 to detect a true effect and at an
a
value equal to 0.05
with a minimal sample 10 in each intervention group. We enrolled 59 patients
with CAD in this study; eight subjects declined to participate. Fifty-one subjects
were randomly assigned to one of three groups: a placebo group (n ¼ 14) or one
of two coenzyme Q10-supplemented groups (60 mg/d, Q10-60 group, n ¼ 19; 150
mg/d, Q10-150 group, n ¼ 18; Fig. 1). Four postmenopausal women who were not
using hormone therapy were recruited into this study. The coenzyme Q10 and
placebo (starch) capsules were commercially available preparations (New Health
Products Co., Ltd., Taichung, Taiwan). The intervention was administered for 12
wk (3 mo). Patients were instructed to take one capsule daily. To monitor
compliance, the researchers reminded patients to check the capsule bag every 4
wk to conrm that the bag was empty. The age, blood pressures, and smoking
habits of the subjects were recorded. Body weight and height were measured,
and then the body mass index (kilograms per meter squared) was calculated.
Laboratory analyses
Fasting venous blood samples (15 mL) were obtained to estimate hemato-
logic and vitamin statuses. Blood specimens were collected in Vacutainer tubes
(Becton Dickinson, Rutherford, NJ, USA) containing ethylenediaminetetraacetic
acid as an anticoagulant or no anticoagulant, as required. Serum and plasma were
prepared and then stored frozen (80
C) until analysis. Hematologic entities (i.e.,
serum urea nitrogen, serum creatinine, total cholesterol, triacylglycerol, low-
density lipoprotein, and high-density lipoprotein) were measured using an
automated biochemical analyzer. An automated hs-CRP measurement was
performed by particle-enhanced immunonephelometry with an Immage
analyzer (Beckman Coulter, Fullerton, CA, USA). The quantitative measurement of
the plasma IL-6 level was performed by an enzyme-linked immunosorbent assay
using commercially available kits (GEN-PROBE, Diaclone, Besancon Cedex,
France) and according to the instructions available from the supplier.
Plasma coenzyme Q10 was measured using high-performance liquid chro-
matography according to the method of Chu et al. [17] and Littarru et al. [18]. The
mean intra- and interassay coefcients of fasting plasma coenzyme Q10 vari-
ability were 1.8% and 4.4%, respectively. The mean analytical recovery of plasma
coenzyme Q10 was 99.8%. Plasma homocysteine was also determined by high-
performance liquid chromatography, as previously described [19]. The mean
intra- and interassay coefcients of fasting plasma homocysteine variability were
1.0% and 4.3%, respectively. The mean analytical recovery of plasma homo-
cysteine was 98.9%.
Plasma malondialdehyde (MDA) was determined using the thiobarbituric
acid-reactive substances method, as described by Botsoglou [20]. Red blood cells
were diluted with 25 sodium phosphate buffer for the superoxide dismutase
(SOD) measurement [21]. The protein contents of plasma and red blood cells
were determined based on the Biuret reaction of the bicinchoninic acid kit
(Thermo, Rockford, IL, USA). The MDA levels were expressed in nanomoles per
milligram of protein and the SOD level was expressed in units per milligram of
protein. All analyses were performed in duplicate.
Statistical analyses
Data were analyzed with SigmaStat 2.03 (Jandel Scientic, San Rafael, CA,
USA). The normal distribution of variables was tested by the Kolmogorov
Smirnov test. Differences in subjects demographic data and hematologic
measurement data among the three intervention groups were analyzed by one-
way analysis of variance or the KruskalWallis analysis of variance on ranks; the
Tukey post hoc test was then used to assess the statistically signicant differ-
ences among groups. Paired t test or the Wilcoxon signed rank test was used to
analyze the data within each group before and after the intervention. For cate-
gorical response variables, differences among the three groups were assessed by
chi-square test or the Fisher exact test. To examine the relation of coenzyme Q10
concentration to the inammatory markers and the MDA and SOD levels before
and after the supplementation, the Pearson product-moment correlation or the
Spearman rank-order correlation was used. Results were considered statistically
signicant at P < 0.05. Values are presented in the text as mean standard
deviation.
Results
Table 1 presents the demographic data and health charac-
teristics of the subjects. There were no signicant differences
among the three groups with respect to age, body mass index,
blood pressure, anthropometric measurements, hematologic
entities (i.e., serum urea nitrogen, serum creatinine, and lipid
proles), and the frequency of smoking at baseline.
The effect of the coenzyme Q10 supplementation on the
inammation markers, lipid peroxidation, and antioxidant
enzyme activities is presented in Figure 2. The plasma coenzyme
Q10 concentration was signicantly increased after the coen-
zyme Q10 supplementation at the dosages of 60 mg/d (P ¼ 0.03)
and 150 mg/d (P < 0.01). After 12 wk of the intervention, the
inammatory markers (IL-6, P ¼ 0.03) were signicantly
decreased in the Q10-150 group. Subjects in the Q10-150 group
had signicantly lower MDA levels and those in the Q10-60 (P ¼
0.05) and Q10-150 (P ¼ 0.06) groups had greater SOD activities.
The correlations among the coenzyme Q10 concentration,
inammatory markers, lipid peroxidation, and antioxidant
enzyme activities are presented in Table 2. Plasma coenzyme Q10
was inversely correlated with hs-CRP (r ¼0.20, P ¼ 0.07) and
IL-6 (r ¼0.25, P ¼ 0.03) at baseline. After 12 wk of supple-
mentation, plasma coenzyme Q10 was signicantly correlated
with MDA (r ¼0.35, P < 0.01) and SOD (r ¼ 0.52, P < 0.01)
activities but not with the inammatory markers. However,
there was no correlation of coenzyme Q10 with homocysteine.
Discussion
A high inammation has been associated with CAD, but few
clinical studies have examined the effect of coenzyme Q10
supplementation on inammation markers. With respect to
inammatory makers, the IL-6 levels were signicantdecreased by
14% after the coenzyme Q10 supplementation at dosage of 150 mg/
d(Fi
g. 2). However, there wasno inuence on the hs-CRP level after
the coenzyme Q10 supplementation. High-sensitivity CRP is
a product of hepatic stimulation and inammation and is under
the regulation of IL-6 [10,22]; IL-6 is a messenger cytokine
(proinammatory cytokine) that is secreted by macrophages and
smooth muscle cells in the atherosclerotic lesion. Thus, IL-6 may
reect inammatory reactions with more sensitivity than hs-CRP
[23,24]. We tried to stratify the inammation status according to
the levels of hs-CRP (0.1 mg/dL) or IL-6 (1.5 pg/mL) as a cutoff
B.-J. Lee et al. / Nutrition 28 (2012) 767772768
point to dene a higher inammation status, which is an average
risk factor for CAD [25,26]. It wasinteresting to nd that the hs-CRP
and IL-6 levels were signicantly lower in those who received
coenzyme Q10 supplementation at a dosage of 150 mg (n ¼ 11,
hs-CRP 0.3 0.3 to 0.2 0.3 mg/dL, P ¼ 0.03; IL-6 1.5 1.5 to 1.2
1.0 pg/mL, P ¼ 0.02; data not shown). Plasma coenzyme Q10
concentration was correlated with the hs-CRP and IL-6 levels at
baseline; however, after the intervention, plasma coenzyme Q10
was signicantly correlated with MDA (r ¼0.35, P < 0.01) and
SOD (r ¼ 0.52, P < 0.01) activities but was not related to the hs-CRP
or IL-6 levels (Table 2). Gökbel et al. [16] reported that coenzyme
Q10 supplements at a dose of 100 mg/d had no signicant effect on
inammation markers in healthy subjects. This lack of an effect in
healthy subjects may be caused by the fact that healthy subjects do
not have high levels of inammation or the dosage of coenzyme
Q10 supplements (100 mg/d) was not high enough to observe an
anti-inammatory effect. Also, in this study of subjects with CAD,
the coenzyme Q10 supplements at a dosage of up to 150 mg/d
produced a slightly anti-inammatory effect on IL-6 but not on
hs-CRP and homocysteine concentrations.
Assessed for eligibility (n=59)
Excluded (n=8)
-Not meeting inclusion criteria (n=0)
-Declined to participate (n=8)
-Other reasons (n=0)
Analysed (n=12)
Placebo group (n=12)
-Excluded from analysis (n=0)
Lost to follow-up (n=2)
-Discontinued intervention (n=2)
Allocated to intervention (n=14):
-Received allocated Placebo group (n=14)
-Did not receive allocated intervention (n=0)
Lost to follow-up (n=6)
-Discontinued intervention: (n=6)
- 60 mg/day (n=3); 150 mg/day (n=3)
Allocated to intervention (n=37)
-Received allocated Coenzyme Q10 supplements:
Q10-60 group (n=19); Q10-150 group (n=18)
-Did not receive allocated intervention (n=0)
Analysed (n=28)
60 mg/day (n=14) and 150 mg/day (n=14)
-Excluded from analysis (n=3)
- 60 mg/day (n=2); 150 mg/day (n=1)
Allocation
Analysis
Follow-Up
Randomized (n=51)
Enrollment
Fig. 1. Flow diagram. Q1060, coenzyme Q10 60 mg/d; Q10-150, coenzyme Q10 150 mg/d.
Table 1
General baseline characteristics of subjects
Placebo (n ¼ 12) Q10-60 (n ¼ 14) Q10-150 (n ¼ 14) P
Men/women 12/0 12/2 13/1 0.39
Age (y) 77.2 7.4 75.1 4.9 79.2 5.4 0.20
Systolic blood pressure (mmHg) 136.7 13.3 132.3 13.3 130.7 8.3 0.72
Diastolic blood pressure (mmHg) 73.3 6.5 75.4 14.9 72.4 5.5 0.84
Body mass index (kg/m
2
) 26.9 2.8 25.6 2.8 25.2 2.6 0.26
Waist-to-hip ratio 0.8 1.0 0.9 0.1 0.9 0.1 0.95
BUN (mmol/L) 14.4 4.3 16.9 5.9 15.8 6.6 0.50
Serum creatinine (
m
mol/L) 114.9 26.5 123.8 44.2 123.8 26.5 0.70
TC (mmol/L) 4.7 0.8 4.9 0.7 5.3 0.8 0.16
TG (mmol/L) 1.5 0.6 1.7 1.2 1.5 1.0 0.80
LDL-C (mmol/L) 3.1 0.9 3.1 0.7 3.5 0.9 0.28
HDL-C (mmol/L) 0.9 0.2 1.0 0.2 1.0 0.3 0.88
Current smoker
*
1 (8.3%) 4 (28.6%) 2 (14.3%) 0.98
Former smoker 4 (33.3%) 2 (14.3%) 3 (21.4%) 0.60
BUN, serum urea nitrogen; HDL-C, high-density lipoprotein cholesterol; hs-CRP, high-sensitivity C-reactive protein; LDL-C, low-density lipoprotein cholesterol; Q10-60,
coenzyme Q10-60 mg/d; Q10-150, coenzyme Q10-150 mg/d; TC, total cholesterol; TG, triacylglycerol
Values are presented as number of subjects (percentage) or mean SD.
*
Currently smoking at least one cigarette per day.
B.-J. Lee et al. / Nutrition 28 (2012) 767772 769
Cell culture experiments have demonstrated that coenzyme
Q10 can moderate the anti-inammatory effects of antioxidant
activities [27] and by nuclear factor-
k
B1dependent gene
expression [28]. In the present study, coenzyme Q10 supple-
ments at a dose of 150 mg showed a signicant antioxidization
effect in decreasing the MDA level (P ¼ 0.03) and slightly
increasing SOD activities (P ¼ 0.06) after 12 wk of intervention. In
addition, the plasma coenzyme Q10 concentration was signi-
cantly correlated with MDA and SOD (P < 0.01; Table 2)atweek
12. Notably, the activities of SOD were signicantly decreased in
the placebo group compared with baseline (P ¼ 0.02) and among
the three groups (P ¼ 0.06). The role of antioxidant enzyme
defenses against the reactive oxygen species is controversial. In
patients with CAD, SOD plays an important role in the protection
of cells against oxidative stress by ameliorating the superoxide
anion [29,30]. Coenzyme Q10 may assist SOD in the uptake of the
superoxide radical to form oxygen and hydrogen peroxide. As
a result, the protective effects of endogenous enzymatic antiox-
idants might decrease in patients with CAD [5,30,31] without
coenzyme Q10 supplementation.
Hyperhomocysteinemia is an independent risk factor of CAD
[32]. Sixty percent of patients with CAD in this study had
hyperhomocysteinemia (15
m
mol/L). However, homocysteine
concentrations were unchanged after the coenzyme Q10
supplementation. A lower homocysteine concentration might
correlate with the status of B vitamins [33]. Among B vitamins,
vitamin B6 (as pyridoxal 5
0
-phosphate) is essential for the
synthesis of coenzyme Q10 [34]. Coenzyme Q10 supplementa-
tion and concurrent supplementation with B vitamins (vitamin
B6) not only provided a better endogenous synthesis of coen-
zyme Q10 [35] but also decreased the homocysteine concentra-
tion [36]. In a coadministration study, patients with breast
cancer treated with enzyme Q10 (100 mg) and B vitamins
(riboavin 10 mg and niacin 50 mg) for 90 d had a signicantly
lower levels of serum cytokines, including IL-1
b
, IL-6, IL-8, and
tumor necrosis factor-
a
(P < 0.05) [37]. Because atherosclerosis is
a chronic inammatory disease, to lower the inammation status
of an individual, a multivitamin supplementation might provide
a greater anti-inammatory effect than a single vitamin
supplementation.
Our study has several limitations. First, the number of
participants was small, and the patients with CAD were stable. Of
the subjects in the present study, 33% had a high inammation
status according to the level of hs-CRP (0.3 mg/dL) and 35%
0.00
0.20
0.40
0.60
0.80
1.00
1.20
Q10-60
Groups
Week 0
Week 12
Placebo
Q10-150
b,*
a,b,*
a
0.00
0.10
0.20
0.30
0.40
0.50
0.60
0.70
Q10-60
Groups
Week 0
Week 12
Placebo
Q10-150
0.00
0.50
1.00
1.50
2.00
2.50
3.00
Q10-60
Groups
Week 0
Week 12
Placebo
Q10-150
*
0
5
10
15
20
25
30
Q10-60
Groups
Week 0
Week 12
Placebo
Q10-150
0
10
20
30
40
50
60
70
80
Q10-60
Groups
Week 0
Week 12
Placebo
Q10-150
*
0
10
20
30
40
50
60
Q10-60
Groups
Week 0
Week 12
Placebo
Q10-150
*
*
*
Fig. 2. Concentration of plasma coenzyme Q10, inammatory markers, lipid peroxidation, and antioxidant enzyme activities after intervention.
*
Values were signicantly
different after the intervention within the group. Values with different superscript letters were signicantly different among the three groups (P < 0.05). hs-CRP, high-
sensitivity C-reactive protein; MDA, malondialdehyde; Q1060, coenzyme Q10 60 mg/d; Q10-150, coenzyme Q10 150 mg/d; SOD, superoxide dism utase.
B.-J. Lee et al. / Nutrition 28 (2012) 767772770
according to the level of IL-6 (1.5 pg/mL). The levels of hs-CRP
and IL-6 showed relatively small differences within the groups
after supplementation, and this may have contributed to the
observed null effect of antioxidants on the inammatory
markers [38,39]. Second, the intervention duration was not long
enough to observe a signicant anti-inammatory effect for this
dosage of coenzyme Q10 supplements (150 mg/d). Long-term
studies are needed to establish the benecial effects of
higher-dosage coenzyme Q10 supplementation on inammation
in patients with CAD.
Acknowledgments
The authors express their sincere appreciation to the subjects
for their participation and to Dr. Hsia who kindly provided the
coenzyme Q10 supplements for this trial. They thank the nurses
at the Taichung Veterans General Hospital and the technical
advisor of the Taipei Institute of Pathology for providing expert
assistance in blood sample collection and data analysis.
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Table 2
Correlations among coenzyme Q10 concentration, inammatory markers, lipid
peroxidation, and antioxidant enzyme activities in 40 subjects
Plasma coenzyme Q10 (
m
mol/L), r (P)
Week 0 Week 12
D
12-0
hs-CRP (mg/mL)
Week 0 0.20 (0.07) dd
Week 12 d 0.14 (0.22) d
D
12-0 dd 0.13 (0.25)
Interleukin-6 (pg/mL)
Week 0 0.25
*
(0.03) dd
Week 12 d 0.07 (0.55) d
D
12-0 dd 0.16 (0.18)
Homocysteine (
m
mol/L)
Week 0 0.04 (0.74) dd
Week 12 d 0.04 (0.71) d
D
12-0 dd 0.07 (0.57)
MDA (nmol/mg protein)
Week 0 0.01 (0.91) dd
Week 12 d 0.35
*
(<0.01) d
D
12-0 dd 0.07 (0.54)
SOD (unit/mg protein)
Week 0 0.04 (0.75) dd
Week 12 d 0.52
*
(<0.01) d
D
12-0 d 0.22 (0.11)
D
12-0, change from week 0 to week 12; MDA, malondialdehyde; hs-CRP, high-
sensitivity C-reactive protein; r, correlation coefcient; SOD, superoxide
dismutase
*
P < 0.05.
B.-J. Lee et al. / Nutrition 28 (2012) 767772 771
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B.-J. Lee et al. / Nutrition 28 (2012) 767772772
    • "On the contrary, inflammation is associated with an increase in circulating levels of Lp(a) [35,36], whereas inhibition of IL-6 signalling decreases serum Lp(a) levels [37] and inhibits apolipoprotein(a) expression and Lp(a) synthesis [38]. Because CoQ 10 can have anti-inflammatory effects [39,40], we might speculate that Lp(a) reduction following CoQ 10 supplemetation might be a consequence of its anti-inflammatory activity. This explanation remains however elusive and need specific demonstration. "
    [Show abstract] [Hide abstract] ABSTRACT: Plasma lipoprotein(a) [Lp(a)] elevations are associated with increased cardiovascular risk. Coenzyme Q10 (CoQ10) is a member of the mitochondrial respiratory chain with a prominent role as a potent gene regulator. The Lp(a)-lowering efficacy of CoQ10 has been investigated in different clinical settings with contrasting results. A systematic literature search in Medline, SCOPUS, Web of Science and Google Scholar databases was conducted to identify controlled trials investigating the efficacy of CoQ10 supplementation on plasma Lp(a) levels. Inverse variance-weighted mean differences (WMDs) and 95% confidence intervals (CIs) were calculated for net changes in Lp(a) levels using a random-effects model. Random-effects meta-regression was performed to assess the effect of putative confounders on plasma Lp(a) levels. Seven randomized controlled trials with a total of 409 subjects (206 in the CoQ10 arm and 203 in the control arm) met the eligibility criteria. Overall, CoQ10 supplementation was paralleled by a slight but significant reduction of plasma Lp(a) levels (WMD: -3.54 mgl/dL, 95% CI: -5.50, -1.58; p<0.001), this effect being more robust in those trials with higher baseline Lp(a) levels (slope: -0.44; 95% CI: -0.80, -0.08; p=0.018). Reduction of plasma Lp(a) levels was consistent across different CoQ10 doses, with an inverse association between administered CoQ10 dose and Lp(a) lowering (slope: 0.04; 95% CI: 0.01, 0.07; p=0.004). Neither total cholesterol and cholesterol subfractions, nor triglyceride levels were affected by CoQ10 supplementation. In conclusion, CoQ10 supplementation, in the tested range of doses, reduces plasma Lp(a) concentrations, particularly in patients with Lp(a)≥30mg/dL. Other lipid indices were not altered by CoQ10 supplementation.
    Full-text · Article · Feb 2016
    • "Bessler illustrated Q10's reductive effect on TNF-α in monocytes; Lee demonstrated Q10's (with a dosage equal to 300 mg) reductive effect on the amount of TNF-α. It is worth mentioning that, prescribing 150 mg of coenzyme Q10, Lee et al. in another study observed no significant difference in the amount of TNF-α, just like in our study [19]. Therefore the difference between the findings of the two studies could be caused by prescribed dosage. "
    [Show abstract] [Hide abstract] ABSTRACT: Introduction: There is considerable evidence that hypertension may increase the levels of cytokines via endothelial stimulation and may stimulate inflammatory reactions. The purpose of this study was to evaluate the effect of oral coenzyme Q10 supplementation on pro-inflammatory factors and adiponectin in mildly hypertensive patients. Methods: This 12-week randomized, double-blind, placebo-controlled clinical trial was carried out during 2012-2013 in Yazd. Sixty mildly hypertensive patients were randomly divided into two groups: placebo (PG, n=30) and coenzyme Q10 (QG, n=30). The QG was given 1 capsule containing 100 mg Q10 per day. The PG was given 1 capsule of the same size and color as the Q10 capsules, but it contained 100 mg of lactose. Plasma pro-inflammatory factors (IL6, IL2, and TNF-alpha), adiponectin, and hs-CRP were determined before and after the intervention. Results: The mean enhancement in adiponectin of QG was significantly higher than PG (from 21.1 +/- 14.5 to 24.2 +/- 15.5 ng/ml, P = 0.04). Significant declines in the median of IL6 (from 23 to 16 pg/ml, P = 0.001) and in the mean of hs-CRP were also observed in QG after intervention (from 3.53 +/- 3.36 to 2.62 +/- 2.51 mg/L, P = 0.03). In the two groups, no significant statistical changes were seen in the median of TNF-alpha and IL2. Conclusion: Daily supplementation of 100 mg coenzyme Q10 can be effective in decreasing some pro-inflammatory factors, such as IL6 and hs-CRP, and in increasing adiponectin.
    Article · Dec 2015
    • "Despite the fact that CoQ 9 is the endogenous form in rats and mice, with just a few exceptions (see below), investigations with animals have used CoQ 10 as the dietary supplement. Dietary supplementation with CoQ 10 (300 mg/day for 12 days) has been found to reduce serum markers of oxidative stress in young swimmers [59] and, in a series of studies in patients with coronary artery disease (60–300 mg CoQ 10 /day for 12 weeks) , to reduce oxidative stress and increase the activity of antioxidant enzymes as well as lowering inflammation as assessed by plasma levels of inflammatory markers such as tumour necrosis factor (TNF)-α and interleukin (IL)-6 [12,13,60,61]. Similarly, dietary CoQ (diet supplemented with 0.07%–0.7% "
    [Show abstract] [Hide abstract] ABSTRACT: Although non-alcoholic fatty liver disease (NAFLD), characterised by the accumulation of triacylglycerol in the liver, is the most common liver disorder, the causes of its development and progression to the more serious non-alcoholic steatohepatitis (NASH) remain incompletely understood. Oxidative stress has been implicated as a key factor in both these processes, and mitochondrial dysfunction and inflammation are also believed to play a part. Coenzyme Q (CoQ) is a powerful antioxidant found in all cell membranes which has an essential role in mitochondrial respiration and also has anti-inflammatory properties. NAFLD has been shown to be associated with disturbances in plasma and liver CoQ concentrations, but the relationship between these changes and disease development and progression is not yet clear. Dietary supplementation with CoQ has been found to be hepatoprotective and to reduce oxidative stress and inflammation as well as improving mitochondrial dysfunction, suggesting that it may be beneficial in NAFLD. However, studies using animal models or patients with NAFLD have given inconclusive results. Overall, evidence is now emerging to indicate that disturbances in CoQ metabolism are involved in NAFLD development and progression to NASH, and this highlights the need for further studies with human subjects to fully clarify its role.
    Full-text · Article · Dec 2015
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