human
***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: BACKGROUND Although patients with chronic kidney disease ( CKD ) are at increased risk of cardiovascular disease ( CVD ) , the roles of lipid-modifying therapies in decreasing CVD risk are unclear . Our aim is to compare the effects of statin and fibrate therapy on arterial function as a risk marker of CVD . STUDY DESIGN Double-blind , r and omized , placebo-controlled , parallel-group study . SETTING & PARTICIPANTS Ambulatory patients with stages 3 to 5 CKD . INTERVENTION 6 weeks of atorvastatin , 40 mg/d , or gemfibrozil , 600 mg twice daily , with placebo . OUTCOMES & MEASUREMENTS Primary outcome was arterial function assessed by means of endothelial-dependent flow-mediated dilatation ( FMD ) and small-artery compliance ( C2 ) . Secondary outcomes included endothelial-independent glyceryl trinitrate-mediated dilatation ( GTNMD ) , large-artery compliance ( C1 ) , and levels of lipids , lipoproteins , and oxidized low-density lipoprotein , as well as markers of insulin resistance and inflammation . RESULTS Compared with placebo , atorvastatin significantly decreased low-density lipoprotein ( -52 % ) , triglyceride ( -30 % ) , and oxidized low-density lipoprotein levels ( -41 % ; P < 0.0001 ) . Gemfibrozil significantly decreased triglyceride levels ( -40 % ) and increased high-density lipoprotein levels ( + 20 % ; P < 0.0001 ) . Neither atorvastatin nor gemfibrozil had a significant effect on markers of insulin resistance or inflammation . There was no significant change in FMD , GTNMD , or C1 with either atorvastatin or gemfibrozil . There was improvement in C2 with atorvastatin ( + 1.1 mL/mm Hg x 100 ) compared with placebo ( P = 0.024 ) , but not with gemfibrozil compared with placebo . LIMITATIONS Small sample size leading to inadequate power , short duration of therapy , and use of a heterogeneous group of patients with CKD and dialysis patients . CONCLUSION In patients with advanced CKD , atorvastatin is associated with improvement in dyslipidemia and small-artery stiffness , but not endothelial function .  Gemfibrozil improves dyslipidemia , but has no effect on arterial function This study aim ed to compare the effects of ω-3 fatty acids and fibrate treatment on plasma levels and activities of hemostatic risk factors on glucose and lipid metabolism in subjects with isolated hypertriglyceridemia . Seventy-three subjects with elevated triglyceride levels were allocated into one of the following treatment options : bezafibrate ( 200 mg twice daily ) , ω-3 fatty acids ( 1 g twice daily ) or placebo . Plasma lipids , glucose homeostasis markers ( fasting and 2-h post-glucose load plasma glucose levels and HOMA ) , as well as plasma levels/activities of fibrinogen , factor VII and PAI-1 were determined at baseline , on the day of r and omization , and after 4 and 12 weeks of the treatment . Not only did bezafibrate  improve plasma lipids , but it also increased glucose sensitivity and tended to reduce post-glucose loads of plasma glucose . Except for the reduction in plasma triglycerides , ω-3 fatty acids produced no effect on the lipid profile and insulin sensitivity . Both treatment options reduced , to similar extents , plasma levels of fibrinogen and PAI-1 and factor VII coagulant activity . Our study indicates that , although fibrates exhibit more-pronounced metabolic effects than do ω-3 fatty acids , both these treatment options are equipotent in producing a complex beneficial effect on hemostasis in isolated hypertriglyceridemic subjects Purpose The aim of this study was to compare the effects of fibrates and omega-3 fatty acids on lymphocyte secretory function and systemic inflammation in patients with isolated hypertriglyceridemia . Methods The study included 107 patients with isolated hypertriglyceridemia who received bezafibrate ( 200 mg twice daily ) , omega-3 fatty acids ( 1 g twice daily ) or placebo for 12 weeks .  The lipid profile , fasting and 2-h post-glucose load plasma glucose levels , homeostasis model assessment index ( HOMA ) , plasma high-sensitivity C-reactive protein ( hsCRP ) levels and lymphocyte release of interleukin-2 , interferon-γ and tumor necrosis factor-α were assessed at baseline , on the day of r and omization , and after 4 and 12 weeks of treatment . Results Both bezafibrate and omega-3 fatty acids reduced plasma triglyceride levels . Bezafibrate additionally decreased total and low-density lipoprotein-cholesterol levels and the HOMA and insignificantly decreased post-glucose load plasma glucose , as well as increased high-density lipoprotein-cholesterol . Bezafibrate treatment was associated with a reduction in lymphocyte release of interleukin-2 , interferon-γ and tumor necrosis factor-α , which was accompanied by a reduction in plasma hsCRP levels .  Omega-3 fatty acid did not significantly reduce lymphocyte cytokine release and plasma hsCRP . The anti-inflammatory effects of both drugs did not correlate with their action on plasma lipids , but in the case of the former the effect was related to the improvement in insulin sensitivity . Conclusion Our results indicate that bezafibrate is superior to omega-3 fatty acid in inhibiting systemic inflammation and lymphocyte secretory function BACKGROUND Exaggerated postpr and ial lipemia ( PPL ) is a factor in atherogenesis , involving endothelial dysfunction and enhanced oxidative stress . We examined the effect of ciprofibrate therapy on these parameters in type 2 diabetes mellitus . METHODS AND RESULTS Twenty patients entered a 3-month , double-blind , placebo-controlled  study . Each subject was studied fasting and after a fatty meal , at baseline , and after 3 months of treatment .  Glucose and lipid profiles were measured over an 8-hour postpr and ial period . Endothelial function ( flow-mediated endothelium-dependent vasodilatation [ FMD ] ) and oxidative stress ( electron paramagnetic resonance spectroscopy ) were measured after fasting and 4 hours postpr and ially . At baseline , both groups exhibited similar PPL and deterioration in endothelial function . After ciprofibrate , fasting and postpr and ial FMD values were significantly higher ( from 3.8+/-1 . 8 % and 1.8+/-1.3 % to 4.8+/-1.1 % and 3.4+/-1.1 % ; P<0.05 ) . This was mirrored by a fall in fasting and postpr and ial triglycerides ( 3 . 1+/-2.1 and 6.6+/-4.1 mmol/L to 1.5+/-0.8 and 2.8+/-1.3 mmol/L , P<0 . 05 ) . Fasting and postpr and ial HDL cholesterol was also elevated ( 0 . 9+/-0.1 and 0.8+/-0.1 mmol/L and 1.2+/-0.2 and 1.2+/-0.1 mmol/L , P<0 . 05 ) . There were no changes in total or LDL cholesterol . Fasting and postpr and ial triglyceride enrichment of all lipoproteins was attenuated , with cholesterol depletion of VLDL and enrichment of HDL . There were similar postpr and ial increases in oxidative stress in both groups at baseline , which was significantly attenuated by ciprofibrate ( 0.3+/-0.6 versus 1.5+/-1.1 U , P<0.05 ) . CONCLUSIONS This study demonstrates that fibrate therapy improves fasting and postpr and ial endothelial function in type 2 diabetes . Attenuation of PPL and the associated oxidative stress , with increased HDL cholesterol levels , may be important BACKGROUND Diabetes mellitus , impaired fasting glucose level , or insulin resistance are associated with increased risk of cardiovascular disease . OBJECTIVES To determine the efficacy of gemfibrozil in subjects with varying levels of glucose tolerance or hyperinsulinemia and to examine the association between diabetes status and glucose and insulin levels and risk of cardiovascular outcomes . METHODS Subgroup analyses from the Department of Veterans Affairs High-Density Lipoprotein Intervention Trial , a r and omized controlled trial that enrolled 2531 men with coronary heart disease ( CHD ) , a high-density lipoprotein cholesterol level of 40 mg/dL or less ( < /=1.04 mmol/L ) , and a low-density lipoprotein cholesterol level of 140 mg/dL or less ( < /=3.63 mmol/L ) . Subjects received either gemfibrozil ( 1200 mg/d ) or matching placebo and were followed up for an average of 5.1 years . In this article , we report the composite end point ( CHD death , stroke , or myocardial infa rct ion ) . RESULTS Compared with those with a normal fasting glucose level , risk was increased in subjects with known diabetes ( hazard ratio [ HR ] , 1.87 ; 95 % confidence interval [ CI ] , 1.44 - 2.43 ; P = .001 ) and those with newly diagnosed diabetes ( HR , 1.72 ; 95 % CI , 1.10 - 2.68 ; P = .02 ) . In persons without diabetes , a fasting plasma insulin level of 39 micro U/mL or greater ( > /=271 pmol/L ) was associated with a 31 % increased risk of events ( P = .03 ) . Gemfibrozil was effective in persons with diabetes ( risk reduction for composite end point , 32 % ; P = .004 ) . The reduction in CHD death was 41 % ( HR , 0.59 ; 95 % CI , 0.39 - 0.91 ; P = .02 ) . Among individuals without diabetes , gemfibrozil was most efficacious for those in the highest fasting plasma insulin level quartile ( risk reduction , 35 % ; P = .04 ) . CONCLUSION In men with CHD and a low high-density lipoprotein cholesterol level , gemfibrozil use was associated with a reduction in major cardiovascular events in persons with diabetes and in nondiabetic subjects with a high fasting plasma insulin level CONTEXT Nonalcoholic fatty liver disease is associated with risk factors for cardiovascular disease , particularly increased plasma triglyceride ( TG ) concentrations and insulin resistance . Fenofibrate and extended release nicotinic acid ( Niaspan ) are used to treat hypertriglyceridemia and can affect fatty acid oxidation and plasma free fatty acid concentrations , which influence intrahepatic triglyceride ( IHTG ) content and metabolic function . OBJECTIVE The objective of the study was to determine the effects of fenofibrate and nicotinic acid therapy on IHTG content and cardiovascular risk factors . EXPERIMENTAL DESIGN AND MAIN OUTCOME MEASURES : We conducted a r and omized , controlled trial to determine the effects of fenofibrate ( 8 wk , 200 mg/d ) , Niaspan ( 16 wk , 2000 mg/d ) , or placebo ( 8 wk ) on IHTG content , very low-density lipoprotein ( VLDL ) kinetics , and insulin sensitivity . SETTING AND PARTICIPANTS Twenty-seven obese subjects with nonalcoholic fatty liver disease ( body mass index 36 + /- 1 kg/m(2 ) , IHTG 23 + /- 2 % ) were studied at Washington University . RESULTS Neither fenofibrate nor Niaspan affected IHTG content , but both decreased plasma TG , VLDL-TG , and VLDL-apolipoprotein B concentrations ( P < 0.05 ) . Fenofibrate increased VLDL-TG clearance from plasma ( 33 to 54 ml/min ; P < 0.05 ) but not VLDL-TG secretion .  Niaspan decreased VLDL-TG secretion ( 27 to 15 micromol/min ; P < 0.05 ) without affecting clearance . Both fenofibrate and Niaspan decreased VLDL-apolipoprotein B secretion ( 1.6 to 1.2 and 1.3 to 0.9 nmol/min , respectively ; P < 0.05 ) . Niaspan reduced hepatic , adipose tissue , and muscle insulin sensitivity ( P < 0.05 ) , whereas fenofibrate had no effect on insulin action . CONCLUSIONS Fenofibrate and Niaspan decrease plasma VLDL-TG concentration without altering IHTG content . However , the mechanism responsible for the change in VLDL-T 
    Output:
    
agent
Conclusion : This meta‐ analysis has shown that fibrate treatment  significantly decreases fasting plasma glucose , insulin levels , and HOMA‐IR indicating additional clinical therapeutic benefits .
***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: BACKGROUND Although patients with chronic kidney disease ( CKD ) are at increased risk of cardiovascular disease ( CVD ) , the roles of lipid-modifying therapies in decreasing CVD risk are unclear . Our aim is to compare the effects of statin and fibrate therapy on arterial function as a risk marker of CVD . STUDY DESIGN Double-blind , r and omized , placebo-controlled , parallel-group study . SETTING & PARTICIPANTS Ambulatory patients with stages 3 to 5 CKD . INTERVENTION 6 weeks of atorvastatin , 40 mg/d , or gemfibrozil , 600 mg twice daily , with placebo . OUTCOMES & MEASUREMENTS Primary outcome was arterial function assessed by means of endothelial-dependent flow-mediated dilatation ( FMD ) and small-artery compliance ( C2 ) . Secondary outcomes included endothelial-independent glyceryl trinitrate-mediated dilatation ( GTNMD ) , large-artery compliance ( C1 ) , and levels of lipids , lipoproteins , and oxidized low-density lipoprotein , as well as markers of insulin resistance and inflammation . RESULTS Compared with placebo , atorvastatin significantly decreased low-density lipoprotein ( -52 % ) , triglyceride ( -30 % ) , and oxidized low-density lipoprotein levels ( -41 % ; P < 0.0001 ) . Gemfibrozil significantly decreased triglyceride levels ( -40 % ) and increased high-density lipoprotein levels ( + 20 % ; P < 0.0001 ) . Neither atorvastatin nor gemfibrozil had a significant effect on markers of insulin resistance or inflammation . There was no significant change in FMD , GTNMD , or C1 with either atorvastatin or gemfibrozil . There was improvement in C2 with atorvastatin ( + 1.1 mL/mm Hg x 100 ) compared with placebo ( P = 0.024 ) , but not with gemfibrozil compared with placebo . LIMITATIONS Small sample size leading to inadequate power , short duration of therapy , and use of a heterogeneous group of patients with CKD and dialysis patients . CONCLUSION In patients with advanced CKD , atorvastatin is associated with improvement in dyslipidemia and small-artery stiffness , but not endothelial function .  Gemfibrozil improves dyslipidemia , but has no effect on arterial function This study aim ed to compare the effects of ω-3 fatty acids and fibrate treatment on plasma levels and activities of hemostatic risk factors on glucose and lipid metabolism in subjects with isolated hypertriglyceridemia . Seventy-three subjects with elevated triglyceride levels were allocated into one of the following treatment options : bezafibrate ( 200 mg twice daily ) , ω-3 fatty acids ( 1 g twice daily ) or placebo . Plasma lipids , glucose homeostasis markers ( fasting and 2-h post-glucose load plasma glucose levels and HOMA ) , as well as plasma levels/activities of fibrinogen , factor VII and PAI-1 were determined at baseline , on the day of r and omization , and after 4 and 12 weeks of the treatment . Not only did bezafibrate  improve plasma lipids , but it also increased glucose sensitivity and tended to reduce post-glucose loads of plasma glucose . Except for the reduction in plasma triglycerides , ω-3 fatty acids produced no effect on the lipid profile and insulin sensitivity . Both treatment options reduced , to similar extents , plasma levels of fibrinogen and PAI-1 and factor VII coagulant activity . Our study indicates that , although fibrates exhibit more-pronounced metabolic effects than do ω-3 fatty acids , both these treatment options are equipotent in producing a complex beneficial effect on hemostasis in isolated hypertriglyceridemic subjects Purpose The aim of this study was to compare the effects of fibrates and omega-3 fatty acids on lymphocyte secretory function and systemic inflammation in patients with isolated hypertriglyceridemia . Methods The study included 107 patients with isolated hypertriglyceridemia who received bezafibrate ( 200 mg twice daily ) , omega-3 fatty acids ( 1 g twice daily ) or placebo for 12 weeks .  The lipid profile , fasting and 2-h post-glucose load plasma glucose levels , homeostasis model assessment index ( HOMA ) , plasma high-sensitivity C-reactive protein ( hsCRP ) levels and lymphocyte release of interleukin-2 , interferon-γ and tumor necrosis factor-α were assessed at baseline , on the day of r and omization , and after 4 and 12 weeks of treatment . Results Both bezafibrate and omega-3 fatty acids reduced plasma triglyceride levels . Bezafibrate additionally decreased total and low-density lipoprotein-cholesterol levels and the HOMA and insignificantly decreased post-glucose load plasma glucose , as well as increased high-density lipoprotein-cholesterol . Bezafibrate treatment was associated with a reduction in lymphocyte release of interleukin-2 , interferon-γ and tumor necrosis factor-α , which was accompanied by a reduction in plasma hsCRP levels .  Omega-3 fatty acid did not significantly reduce lymphocyte cytokine release and plasma hsCRP . The anti-inflammatory effects of both drugs did not correlate with their action on plasma lipids , but in the case of the former the effect was related to the improvement in insulin sensitivity . Conclusion Our results indicate that bezafibrate is superior to omega-3 fatty acid in inhibiting systemic inflammation and lymphocyte secretory function BACKGROUND Exaggerated postpr and ial lipemia ( PPL ) is a factor in atherogenesis , involving endothelial dysfunction and enhanced oxidative stress . We examined the effect of ciprofibrate therapy on these parameters in type 2 diabetes mellitus . METHODS AND RESULTS Twenty patients entered a 3-month , double-blind , placebo-controlled  study . Each subject was studied fasting and after a fatty meal , at baseline , and after 3 months of treatment .  Glucose and lipid profiles were measured over an 8-hour postpr and ial period . Endothelial function ( flow-mediated endothelium-dependent vasodilatation [ FMD ] ) and oxidative stress ( electron paramagnetic resonance spectroscopy ) were measured after fasting and 4 hours postpr and ially . At baseline , both groups exhibited similar PPL and deterioration in endothelial function . After ciprofibrate , fasting and postpr and ial FMD values were significantly higher ( from 3.8+/-1 . 8 % and 1.8+/-1.3 % to 4.8+/-1.1 % and 3.4+/-1.1 % ; P<0.05 ) . This was mirrored by a fall in fasting and postpr and ial triglycerides ( 3 . 1+/-2.1 and 6.6+/-4.1 mmol/L to 1.5+/-0.8 and 2.8+/-1.3 mmol/L , P<0 . 05 ) . Fasting and postpr and ial HDL cholesterol was also elevated ( 0 . 9+/-0.1 and 0.8+/-0.1 mmol/L and 1.2+/-0.2 and 1.2+/-0.1 mmol/L , P<0 . 05 ) . There were no changes in total or LDL cholesterol . Fasting and postpr and ial triglyceride enrichment of all lipoproteins was attenuated , with cholesterol depletion of VLDL and enrichment of HDL . There were similar postpr and ial increases in oxidative stress in both groups at baseline , which was significantly attenuated by ciprofibrate ( 0.3+/-0.6 versus 1.5+/-1.1 U , P<0.05 ) . CONCLUSIONS This study demonstrates that fibrate therapy improves fasting and postpr and ial endothelial function in type 2 diabetes . Attenuation of PPL and the associated oxidative stress , with increased HDL cholesterol levels , may be important BACKGROUND Diabetes mellitus , impaired fasting glucose level , or insulin resistance are associated with increased risk of cardiovascular disease . OBJECTIVES To determine the efficacy of gemfibrozil in subjects with varying levels of glucose tolerance or hyperinsulinemia and to examine the association between diabetes status and glucose and insulin levels and risk of cardiovascular outcomes . METHODS Subgroup analyses from the Department of Veterans Affairs High-Density Lipoprotein Intervention Trial , a r and omized controlled trial that enrolled 2531 men with coronary heart disease ( CHD ) , a high-density lipoprotein cholesterol level of 40 mg/dL or less ( < /=1.04 mmol/L ) , and a low-density lipoprotein cholesterol level of 140 mg/dL or less ( < /=3.63 mmol/L ) . Subjects received either gemfibrozil ( 1200 mg/d ) or matching placebo and were followed up for an average of 5.1 years . In this article , we report the composite end point ( CHD death , stroke , or myocardial infa rct ion ) . RESULTS Compared with those with a normal fasting glucose level , risk was increased in subjects with known diabetes ( hazard ratio [ HR ] , 1.87 ; 95 % confidence interval [ CI ] , 1.44 - 2.43 ; P = .001 ) and those with newly diagnosed diabetes ( HR , 1.72 ; 95 % CI , 1.10 - 2.68 ; P = .02 ) . In persons without diabetes , a fasting plasma insulin level of 39 micro U/mL or greater ( > /=271 pmol/L ) was associated with a 31 % increased risk of events ( P = .03 ) . Gemfibrozil was effective in persons with diabetes ( risk reduction for composite end point , 32 % ; P = .004 ) . The reduction in CHD death was 41 % ( HR , 0.59 ; 95 % CI , 0.39 - 0.91 ; P = .02 ) . Among individuals without diabetes , gemfibrozil was most efficacious for those in the highest fasting plasma insulin level quartile ( risk reduction , 35 % ; P = .04 ) . CONCLUSION In men with CHD and a low high-density lipoprotein cholesterol level , gemfibrozil use was associated with a reduction in major cardiovascular events in persons with diabetes and in nondiabetic subjects with a high fasting plasma insulin level CONTEXT Nonalcoholic fatty liver disease is associated with risk factors for cardiovascular disease , particularly increased plasma triglyceride ( TG ) concentrations and insulin resistance . Fenofibrate and extended release nicotinic acid ( Niaspan ) are used to treat hypertriglyceridemia and can affect fatty acid oxidation and plasma free fatty acid concentrations , which influence intrahepatic triglyceride ( IHTG ) content and metabolic function . OBJECTIVE The objective of the study was to determine the effects of fenofibrate and nicotinic acid therapy on IHTG content and cardiovascular risk factors . EXPERIMENTAL DESIGN AND MAIN OUTCOME MEASURES : We conducted a r and omized , controlled trial to determine the effects of fenofibrate ( 8 wk , 200 mg/d ) , Niaspan ( 16 wk , 2000 mg/d ) , or placebo ( 8 wk ) on IHTG content , very low-density lipoprotein ( VLDL ) kinetics , and insulin sensitivity . SETTING AND PARTICIPANTS Twenty-seven obese subjects with nonalcoholic fatty liver disease ( body mass index 36 + /- 1 kg/m(2 ) , IHTG 23 + /- 2 % ) were studied at Washington University . RESULTS Neither fenofibrate nor Niaspan affected IHTG content , but both decreased plasma TG , VLDL-TG , and VLDL-apolipoprotein B concentrations ( P < 0.05 ) . Fenofibrate increased VLDL-TG clearance from plasma ( 33 to 54 ml/min ; P < 0.05 ) but not VLDL-TG secretion .  Niaspan decreased VLDL-TG secretion ( 27 to 15 micromol/min ; P < 0.05 ) without affecting clearance . Both fenofibrate and Niaspan decreased VLDL-apolipoprotein B secretion ( 1.6 to 1.2 and 1.3 to 0.9 nmol/min , respectively ; P < 0.05 ) . Niaspan reduced hepatic , adipose tissue , and muscle insulin sensitivity ( P < 0.05 ) , whereas fenofibrate had no effect on insulin action . CONCLUSIONS Fenofibrate and Niaspan decrease plasma VLDL-TG concentration without altering IHTG content . However , the mechanism responsible for the change in VLDL-T 
    Output:
    