***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE —To investigate the effects of fenofibrate and coenzyme Q10 ( CoQ ) on diastolic function , ambulatory blood pressure ( ABP ) , and heart rate ( HR ) in type 2 diabetic subjects with left ventricular diastolic dysfunction ( LVDD ) . RESEARCH DESIGN AND METHODS —We r and omized , double-blind , 74 subjects to fenofibrate 160 mg daily , CoQ 200 mg daily , fenofibrate 160 mg plus CoQ 200 mg daily , or matching placebo for 6 months . Echocardiography ( including tissue Doppler imaging ) and 24-h ABP and HR monitoring were performed pre- and postintervention . RESULTS —Neither fenofibrate nor CoQ , alone or in combination , altered early diastolic mitral annular myocardial relaxation velocity ( E′ ) , early-to-late mitral inflow velocity ratio ( E/A ) , deceleration time , isovolumic relaxation time , or the ratio of early mitral flow velocity to early diastolic mitral annular myocardial relaxation velocity ( E/E′ ) compared with placebo ( P > 0.05 ) . Fenofibrate and CoQ interactively ( P = 0.001 ) lowered 24-h systolic blood pressure ( −3.4 ± 0.09 mmHg , P = 0.010 ) , with a prominent nocturnal effect ( −5.7 ± 1.5 mmHg , P = 0.006 ) . Fenofibrate ( −1.3 ± 0.5 mmHg , P = 0.013 ) and CoQ ( −2.2 ± 0.5 mmHg , P < 0.001 ) independently lowered 24-h diastolic blood pressure . Fenofibrate reduced 24-h HR ( −3.3 ± 0.5 beats/min , P < 0.001 ) , but CoQ had no effect on HR . CONCLUSIONS —In type 2 diabetic subjects with LVDD , neither fenofibrate nor CoQ , alone or in combination , improved diastolic function significantly . However , fenofibrate and CoQ independently and interactively lowered 24-h blood pressure , and fenofibrate alone reduced 24-h HR Objective : Our objective was to assess effects of dietary supplementation with coenzyme Q10 ( CoQ ) on blood pressure and glycaemic control in subjects with type 2 diabetes , and to consider oxidative stress as a potential mechanism for any effects . Subjects and design : Seventy-four subjects with uncomplicated type 2 diabetes and dyslipidaemia were involved in a r and omised double blind placebo-controlled 2 × 2 factorial intervention . Setting : The study was performed at the University of Western Australia , Department of Medicine at Royal Perth Hospital , Australia . Interventions : Subjects were r and omly assigned to receive an oral dose of 100 mg CoQ twice daily ( 200 mg/day ) , 200 mg fenofibrate each morning , both or neither for 12 weeks . Main outcome measures : We report an analysis and discussion of the effects of CoQ on blood pressure , on long-term glycaemic control measured by glycated haemoglobin ( HbA1c ) , and on oxidative stress assessed by measurement of plasma F2-isoprostanes . Results : Fenofibrate did not alter blood pressure , HbA1c , or plasma F2-isoprostanes . There was a 3-fold increase in plasma CoQ concentration ( 3.4±0.3 µmol/l , P<0.001 ) as a result of CoQ supplementation . The main effect of CoQ was to significantly decrease systolic ( −6.1±2.6 mmHg , P=0.021 ) and diastolic ( −2.9±1.4 mmHg , P=0.048 ) blood pressure and HbA1c ( −0.37±0.17 % , P=0.032 ) . Plasma F2-isoprostane concentrations were not altered by CoQ ( 0.14±0.15 nmol/l , P=0.345 ) . Conclusions : These results show that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type 2 diabetes , but these improvements were not associated with reduced oxidative stress , as assessed by F2-isoprostanes . Sponsorship : This study was supported by a grant from the NH&MRC , Australia OBJECTIVE The vascular benefits of statins might be attenuated by inhibition of coenzyme Q10 ( CoQ10 ) synthesis . We investigated whether oral CoQ10 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 flow-mediated dilatation [ FMD ] < 5.5 % ) were r and omized to oral CoQ10  ( 200 mg/day ) or placebo for 12 weeks . We measured brachial artery FMD and nitrate-mediated dilatation ( NMD ) by ultrasonography . Plasma F2-isoprostane and 24-h urinary 20-hydroxyeicosatetraenoic acid ( HETE ) levels were measured as systemic oxidative stress markers . RESULTS Compared with placebo , CoQ10 supplementation increased brachial artery FMD by 1.0 ± 0.5 % ( P = 0.04 ) , but did not alter NMD ( P = 0.66 ) . CoQ10 supplementation also did not alter plasma F2-isoprostane ( P = 0.58 ) or urinary 20-HETE levels ( P = 0.28 ) . CONCLUSIONS CoQ10 supplementation improved endothelial dysfunction in statin-treated type 2 diabetic patients , possibly by altering local vascular oxidative stress BACKGROUND Parkinson disease ( PD ) is a degenerative neurological disorder for which no treatment has been shown to slow the progression . OBJECTIVE To determine whether a range of dosages of coenzyme Q10 is safe and well tolerated and could slow the functional decline in PD . DESIGN Multicenter , r and omized , parallel-group , placebo-controlled , double-blind , dosage-ranging trial . SETTING Academic movement disorders clinics . PATIENTS Eighty subjects with early PD who did not require treatment for their disability . INTERVENTIONS R and om assignment to placebo or coenzyme Q10 at dosages of 300 , 600 , or 1200 mg/d . MAIN OUTCOME MEASURE The subjects underwent evaluation with the Unified Parkinson Disease Rating Scale ( UPDRS ) at the screening , baseline , and 1- , 4- , 8- , 12- , and 16-month visits . They were followed up for 16 months or until disability requiring treatment with levodopa had developed . The primary response variable was the change in the total score on the UPDRS from baseline to the last visit . RESULTS The adjusted mean total UPDRS changes were + 11.99 for the placebo group , + 8.81 for the 300-mg/d group , + 10.82 for the 600-mg/d group , and + 6.69 for the 1200-mg/d group . The P value for the primary analysis , a test for a linear trend between the dosage and the mean change in the total UPDRS score , was.09 , which met our prespecified criteria for a positive trend for the trial . A prespecified , secondary analysis was the comparison of each treatment group with the placebo group , and the difference between the 1200-mg/d and placebo groups was significant ( P = .04 ) . CONCLUSIONS Coenzyme Q10 was safe and well tolerated at dosages of up to 1200 mg/d . Less disability developed in subjects assigned to coenzyme Q10 than in those assigned to placebo , and the benefit was greatest in subjects receiving the highest dosage . Coenzyme Q10 appears to slow the progressive deterioration of function in PD , but these results need to be confirmed in a larger study Myalgia is the most frequently reported adverse side effect associated with statin therapy and often necessitates reduction in dose , or the cessation of therapy , compromising cardiovascular risk management . One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10 ) , a key component of the mitochondrial electron transport chain . This pilot study evaluated the effect of coenzyme Q(10 ) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia . Forty-four patients were r and omized to coenzyme Q(10 ) ( 200 mg/day ) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day , doubling every 4 weeks if tolerated to a maximum of 40 mg/day . Patients experiencing significant myalgia reduced their statin dose or discontinued treatment . Myalgia was assessed using a visual analogue scale . There was no difference between combined therapy and statin alone in the myalgia score change ( median 6.0 [ interquartile range 2.1 to 8.8 ] vs 2.3 [ 0 to 12.8 ] , p = 0.63 ) , in the number of patients tolerating simvastatin  40 mg/day ( 16 of 22 [ 73 % ] with coenzyme Q(10 ) vs 13 of 22 [ 59 % ] with placebo , p = 0.34 ) , or in the number of patients remaining on therapy ( 16 of 22 [ 73 % ] with coenzyme Q(10 ) vs 18 of 22 [ 82 % ] with placebo , p = 0.47 ) . In conclusion , coenzyme Q(10 ) supplementation did not improve statin tolerance or myalgia , although further studies are warranted BACKGROUND Oxidative stress and dysregulation of antioxidant function play a pivotal role in the diabetic complications . METHODS Fifty-nine patients with diabetes were r and omly assigned into three groups . 1 ) PL group ( n = 19 ) : Polarized light ( PL ) was applied to neuropathic ulcers of diabetic foot twice daily for ten minutes in pulse regimen during three months . 2 ) QALA group ( n = 20 ) : Antioxidants ( 60 mg hydrosoluble CoQ10 , 100 mg alpha-lipoic acid ( ALA ) and 200 mg vitamin E ) were used in two daily doses for three months . 3 ) QALAPL group ( n = 20 ) : Patients used antioxidants along with PL applications . To test for differences in means , paired Student 's t-test ( before and after three months ) was used . RESULTS Three months application of PL significantly increased plasma concentrations of coenzyme Q10 , alpha-tocopherol , tau-tocopherol and beta-carotene , and decreased lactate dehydrogenase ( LDH ) activity . Supplementation with antioxidants decreased plasma lipid peroxides , increased concentration of CoQ10 and improved echocardiographic parameters . Simultaneous application of PL and antioxidants significantly stimulated plasma CoQ10 and alpha-tocopherol concentrations , decreased LDH activity and contributed to improvement in heart left ventricular function in diabetics . CONCLUSION Thus the data show that supportive therapy with PL along with the antioxidants hydrosoluble CoQ10 , alpha-lipoic acid and vitamin E is an effective way of controlling the complications of type 2 diabetes ( Tab . 7 , Fig. 2 , Ref . 44 ) Arteriopathy is the principal complication of type 2 diabetes mellitus . It develops from endothelial dysfunction , which we have hypothesised occurs in diabetes primarily as a consequence of dyslipidaemia and oxidative stress . Fenofibrate and CoQ may improve endothelial function by regulating dyslipidaemia and oxidative stress , respectively . We therefore aim ed to assess the independent and combined effects of fenofibrate and coenzyme Q(10 ) ( CoQ ) on endothelium-dependent and endothelium-independent vasodilator function of the forearm microcirculation in type 2 diabetes . Eighty dyslipidaemic type 2 diabetics were r and omized to receive fenofibrate ( 200 mg/daily ) , CoQ ( 200 mg/daily ) , fenofibrate plus CoQ ( 200 + 200 mg daily ) , or placebo for 12 weeks . Forearm microcirculatory function was assessed with venous occlusion plethysmography during the infusion of acetylcholine ( ACh ) , bradykinin ( BK ) , sodium nitroprusside ( SNP ) and N(G)-monomethyl-L-arginine ( L-NMMA ) into the brachial artery . Blood flow responses were calculated as area under the curve ( AUC ) . Fenofibrate significantly lowered plasma cholesterol , triglyceride and fibrinogen ( P<0.001 ) , and elevated HDL-cholesterol and homoc 
    Output:
    
Neither CoQ10 alone nor CoQ10 plus fenofibrate  improved glycemic control .
In addition , CoQ10 , alone or in combination with fenofibrate , did not alter LDL-C , HDL-C and blood pressure .
WHAT IS NEW AND CONCLUSIONS CoQ10 supplementation has no beneficial effects on glycemic control , lipid profile or blood pressure in patients with diabetes .
However , it may reduce triglycerides levels .