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 Interleukin-6 ( IL-6 ) plays a central role in inflammation and tissue injury . However , epidemiological data evaluating the role of IL-6 in atherogenesis are sparse . METHODS AND RESULTS In a prospect i ve study involving 14 916 apparently healthy men , we measured baseline plasma concentration of IL-6 in 202 participants who subsequently developed myocardial infa rct ion ( MI ) and in 202 study participants matched for age and smoking status who did not report vascular disease during a 6-year follow-up .  Median concentrations of IL-6 at baseline were higher among men who subsequently had an MI than among those who did not ( 1.81 versus 1 . 46 pg/mL ; P=0.002 ) . The risk of future MI increased with increasing quartiles of baseline IL-6 concentration ( P for trend < 0.001 ) such that men in the highest quartile at entry had a relative risk 2.3 times higher than those in the lowest quartile ( 95 % CI 1.3 to 4.3 , P=0.005 ) ; for each quartile increase in IL-6 , there was a 38 % increase in risk (P=0.001).This relationship remained significant after adjustment for other cardiovascular risk factors , was stable over long periods of follow-up , and was present in all low-risk subgroups , including nonsmokers . Although the strongest correlate of IL-6 in these data was C-reactive protein ( r=0.43 , P<0.001 ) , the relationship of IL-6 with subsequent risk remained after control for this factor ( P<0.001 ) . CONCLUSIONS In apparently healthy men , elevated levels of IL-6 are associated with increased risk of future MI . These data thus support a role for cytokine-mediated inflammation in the early stages of atherogenesis OBJECTIVE Inflammation mediators have been recognized as risk factors for the pathogenesis of coronary artery disease ( CAD ) . The purpose of this study was to investigate the effect of L-carnitine supplementation ( LC , 1000 mg/d ) on inflammation markers in patients with CAD . METHODS We enrolled 47 patients with CAD in the study . The patients with CAD were identified by cardiac catheterization as having < 50 % stenosis of one major coronary artery . The patients were r and omly assigned to the placebo ( n = 24 ) and LC ( n = 23 ) groups and the intervention was administered for 12 wk . The levels of LC , antioxidant status ( malondialdehyde and antioxidant enzymes activities ) , and inflammation markers ( C-reactive protein [ CRP ] , interleukin [IL]-6 , and tumor necrosis factor [TNF]-α ) were measured . RESULTS Thirty-nine participants completed the study ( 19 placebo ; 20 LC ) . After LC supplementation , the levels of inflammation markers were significantly reduced compared with the baseline ( CRP , P < 0.01 ; IL-6 , P = 0.03 ; TNF-α , P = 0.07 ) and those in the placebo group ( CRP , P < 0.05 ; IL-6 , P = 0.04 ; TNF-α , P = 0.03 ) . The levels of inflammation markers were significantly negatively correlated with the levels of LC and antioxidant enzymes activities ( P < 0.05 ) . CONCLUSIONS We suggest that LC supplementation , due to its antioxidant effects , may have potential utility to reduce inflammation in CAD Background Resting and postpr and ial oxidative stress is elevated in those with metabolic disorders such as diabetes .  Antioxidant supplementation may attenuate the rise in oxidative stress following feeding . Therefore we sought to determine the effects of acetyl L-carnitine arginate ( ALCA ) on resting and postpr and ial biomarkers of glucose and lipid metabolism , as well as oxidative stress . Methods Twenty-nine pre-diabetic men and women were r and omly assigned to either 3 g·day-1  of ALCA ( n = 14 ; 31 ± 3 yrs )  or placebo ( n = 15 ; 35 ± 3 yrs ) in a double-blind design , to consume for eight weeks . Fasting blood sample s were taken from subjects both pre and post intervention . After each fasting sample was obtained , subjects consumed a high fat , high carbohydrate meal and additional blood sample s were taken at 1 , 2 , 4 , and 6 hours post meal . Sample s were analyzed for a variety of metabolic variables ( e.g. , glucose , HbA1c , lipid panel , C-reactive protein , nitrate/nitrite , and several markers of oxidative stress ) . Area under the curve ( AUC ) was calculated for each variable measured post meal , both pre and post intervention . Results ALCA , but not placebo , result ed in an increase in nitrate/nitrite ( 25.4 ± 1.9 to 30.1 ± 2.8 μmol·L-1 ) from pre to post intervention , with post intervention values greater compared to placebo ( p = 0.01 ) . No other changes of statistical significance were noted ( p > 0.05 ) , although ALCA result ed in slight improvements in glucose ( 109 ± 5 to 103 ± 5 mg·dL-1 ) , HbA1c ( 6.6 ± 1.1 to 6.2 ± 1.2 % ) , and HOMA-IR ( 3.3 ± 1.3 to 2.9 ± 1.2 ) . AUC postpr and ial data were not statistically different between ALCA and placebo for any variable ( p > 0.05 ) . However , nitrate/nitrite demonstrated a moderate effect size ( r = 0.35 ) for increase from pre ( 139.50 ± 18.35 μmol·L-1·6 hr-1 ) to post ( 172.40 ± 21.75 μmol·L-1·6 hr-1 ) intervention with ALCA , and the magnitude of decrease following feeding was not as pronounced as with placebo . ConclusionS upplementation with ALCA results in an increase in resting nitrate/nitrite in pre-diabetics , without any statistically significant change in other metabolic or oxidative stress variables measured at rest or post meal Background Frailty is a biological syndrome of decreased reserve and resistance to stressors due to decline in multiple physiological systems . Amino acid deficiency , including L-carnitine , has been proposed to be associated with its pathophysiology . Nevertheless , the efficacy of L-carnitine supplementation on frailty status has not been documented . Thus , this study aim ed to determine the effect of 10-week L-carnitine supplement ( 1.5 g/day ) on frailty status and its biomarkers and also physical function , cognition , and nutritional status among prefrail older adults in Klang Valley , Malaysia . Methodology This study is a r and omized , double-blind , placebo-controlled clinical trial conducted among 50 prefrail subjects r and omized into two groups ( 26 in L-carnitine group and 24 in placebo group ) . Outcome measures include frailty status using Fried criteria and Frailty Index accumulation of deficit , selected frailty biomarkers ( interleukin-6 , tumor necrosis factor-alpha , and insulin-like growth factor-1 ) , physical function , cognitive function , nutritional status and biochemical profile . Results The results indicated that the mean scores of Frailty Index score and h and grip test were significantly improved in subjects supplemented with L-carnitine ( P<0.05 for both parameters ) as compared to no change in the placebo group . Based on Fried criteria , four subjects ( three from the L-carnitine group and one from the control group ) transited from prefrail status to robust after the intervention . Conclusion L-carnitine supplementation has a favorable effect on the functional status and fatigue in prefrail older adults The aim of the study was to evaluate the effects of 12-month treatment with sibutramine plus L-carnitine compared with sibutramine alone on body weight , glycemic control , insulin resistance , and inflammatory state in type 2 diabetes mellitus patients . Two hundred fifty-four patients with uncontrolled type 2 diabetes mellitus ( glycated hemoglobin [ HbA(1c ) ] > 8.0 % ) in therapy with different oral hypoglycemic agents or insulin  were enrolled in this study and r and omized to take sibutramine 10 mg plus L-carnitine 2 g or sibutramine 10 mg in monotherapy . We evaluated at baseline and after 3 , 6 , 9 , and 12 months these parameters : body weight , body mass index , HbA(1c ) , fasting plasma glucose , postpr and ial plasma glucose , fasting plasma insulin , homeostasis model assessment of insulin resistance index , total cholesterol , low-density lipoprotein cholesterol , high-density lipoprotein cholesterol , triglycerides , leptin , tumor necrosis factor-α , adiponectin , vaspin , and high-sensitivity C-reactive protein .  Sibutramine plus L-carnitine gave a faster improvement of fasting plasma glucose , postpr and ial plasma glucose , lipid profile , leptin , tumor necrosis factor-α , and high-sensitivity C-reactive protein compared with sibutramine alone . Furthermore , there was a better improvement of body weight , HbA(1c ) , fasting plasma insulin , homeostasis model assessment of insulin resistance index , vaspin , and adiponectin  with sibutramine plus L-carnitine compared with sibutramine alone . Sibutramine plus L-carnitine gave a better and faster improvement of all the analyzed parameters compared with sibutramine alone without giving any severe adverse effect OBJECTIVES : Nonalcoholic steatohepatitis ( NASH ) is a known metabolic disorder of the liver . No treatment has been conclusively shown to improve NASH or prevent disease progression . The function of L-carnitine to modulate lipid profile , glucose metabolism , oxidative stress , and inflammatory responses has been shown . The aim of this study was to evaluate the effects of L-carnitine 's supplementation on regression of NASH . METHODS : In patients with NASH and control subjects , we r and omly dispensed one 1-g L-carnitine tablet after breakfast plus diet and one 1 g tablet after dinner plus diet for 24 weeks or diet alone at the same dosage and regimen . We evaluated liver enzymes , lipid profile , fasting plasma glucose , C-reactive protein ( CRP ) , tumor necrosis factor (TNF)-α , homeostasis model assessment (HOMA)-IR , body mass index , and histological scores . RESULTS : At the end of the study , L-carnitine-treated patients showed significant improvements in the following parameters : aspartate aminotransferase ( P=0.000 ) , alanine aminotransferase ( ALT ) ( P=0.000 ) , γ-glutamyl-transpeptidase ( γ-GT ) ( P=0.000 ) , total cholesterol ( P=0.000 ) , low-density lipoprotein ( LDL ) ( P=0.000 ) , high-density lipoprotein ( HDL ) ( P=0.000 ) , triglycerides ( P=0.000 ) , glucose ( P=0.000 ) , HOMA-IR ( P=0.000 ) , CRP ( P=0.000 ) , TNF-α ( P=0.000 ) , and histological scores ( P=0.000 ) . CONCLUSIONS : L-carnitine supplementation to diet is useful for reducing TNF-α and CRP , and for improving liver function , glucose plasma level , lipid profile , HOMA-IR , and histological manifestations of NASH To evaluate the effects of 1-year treatment with orlistat plus L-carnitine compared to orlistat alone on body weight , glycemic and lipid control , and inflammatory parameters in obese type 2 diabetic patients . Two hundred and fifty-eight patients with uncontrolled type 2 diabetes mellitus ( T2DM ) [ glycated hemoglobin ( HbA(1c ) ) > 8.0 % ] in therapy with different oral hypoglycemic agents or insulin  were enrolled in this study and r and omized to take orlistat 120 mg three times a day plus L-carnitine 2 g one time a day or orlistat 120 mg three times a day . We evaluated the following parameters at baseline and after 3 , 6 , 9 , and 12 months : body weight , body mass index ( BMI ) , glycated hemoglobin ( HbA(1c ) ) , fasting plasma glucose ( FPG ) , postpr and ial plasma glucose ( PPG ) , fasting plasma insulin ( FPI ) , homeostasis model assessment insulin resistance index ( HOMA-IR ) , total cholesterol ( TC ) , low-density lipoprotein cholesterol ( LDL-C ) , high-density lipoprotein cholesterol ( HDL-C ) , triglycerides ( Tg ) , adiponectin ( ADN ) , leptin , tumor ne 
    Output:
    
agent
Conclusion Our results indicate  that L-carnitine  reduced inflammatory mediators , especially in studies with a duration of more than 12 weeks .
***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 Interleukin-6 ( IL-6 ) plays a central role in inflammation and tissue injury . However , epidemiological data evaluating the role of IL-6 in atherogenesis are sparse . METHODS AND RESULTS In a prospect i ve study involving 14 916 apparently healthy men , we measured baseline plasma concentration of IL-6 in 202 participants who subsequently developed myocardial infa rct ion ( MI ) and in 202 study participants matched for age and smoking status who did not report vascular disease during a 6-year follow-up .  Median concentrations of IL-6 at baseline were higher among men who subsequently had an MI than among those who did not ( 1.81 versus 1 . 46 pg/mL ; P=0.002 ) . The risk of future MI increased with increasing quartiles of baseline IL-6 concentration ( P for trend < 0.001 ) such that men in the highest quartile at entry had a relative risk 2.3 times higher than those in the lowest quartile ( 95 % CI 1.3 to 4.3 , P=0.005 ) ; for each quartile increase in IL-6 , there was a 38 % increase in risk (P=0.001).This relationship remained significant after adjustment for other cardiovascular risk factors , was stable over long periods of follow-up , and was present in all low-risk subgroups , including nonsmokers . Although the strongest correlate of IL-6 in these data was C-reactive protein ( r=0.43 , P<0.001 ) , the relationship of IL-6 with subsequent risk remained after control for this factor ( P<0.001 ) . CONCLUSIONS In apparently healthy men , elevated levels of IL-6 are associated with increased risk of future MI . These data thus support a role for cytokine-mediated inflammation in the early stages of atherogenesis OBJECTIVE Inflammation mediators have been recognized as risk factors for the pathogenesis of coronary artery disease ( CAD ) . The purpose of this study was to investigate the effect of L-carnitine supplementation ( LC , 1000 mg/d ) on inflammation markers in patients with CAD . METHODS We enrolled 47 patients with CAD in the study . The patients with CAD were identified by cardiac catheterization as having < 50 % stenosis of one major coronary artery . The patients were r and omly assigned to the placebo ( n = 24 ) and LC ( n = 23 ) groups and the intervention was administered for 12 wk . The levels of LC , antioxidant status ( malondialdehyde and antioxidant enzymes activities ) , and inflammation markers ( C-reactive protein [ CRP ] , interleukin [IL]-6 , and tumor necrosis factor [TNF]-α ) were measured . RESULTS Thirty-nine participants completed the study ( 19 placebo ; 20 LC ) . After LC supplementation , the levels of inflammation markers were significantly reduced compared with the baseline ( CRP , P < 0.01 ; IL-6 , P = 0.03 ; TNF-α , P = 0.07 ) and those in the placebo group ( CRP , P < 0.05 ; IL-6 , P = 0.04 ; TNF-α , P = 0.03 ) . The levels of inflammation markers were significantly negatively correlated with the levels of LC and antioxidant enzymes activities ( P < 0.05 ) . CONCLUSIONS We suggest that LC supplementation , due to its antioxidant effects , may have potential utility to reduce inflammation in CAD Background Resting and postpr and ial oxidative stress is elevated in those with metabolic disorders such as diabetes .  Antioxidant supplementation may attenuate the rise in oxidative stress following feeding . Therefore we sought to determine the effects of acetyl L-carnitine arginate ( ALCA ) on resting and postpr and ial biomarkers of glucose and lipid metabolism , as well as oxidative stress . Methods Twenty-nine pre-diabetic men and women were r and omly assigned to either 3 g·day-1  of ALCA ( n = 14 ; 31 ± 3 yrs )  or placebo ( n = 15 ; 35 ± 3 yrs ) in a double-blind design , to consume for eight weeks . Fasting blood sample s were taken from subjects both pre and post intervention . After each fasting sample was obtained , subjects consumed a high fat , high carbohydrate meal and additional blood sample s were taken at 1 , 2 , 4 , and 6 hours post meal . Sample s were analyzed for a variety of metabolic variables ( e.g. , glucose , HbA1c , lipid panel , C-reactive protein , nitrate/nitrite , and several markers of oxidative stress ) . Area under the curve ( AUC ) was calculated for each variable measured post meal , both pre and post intervention . Results ALCA , but not placebo , result ed in an increase in nitrate/nitrite ( 25.4 ± 1.9 to 30.1 ± 2.8 μmol·L-1 ) from pre to post intervention , with post intervention values greater compared to placebo ( p = 0.01 ) . No other changes of statistical significance were noted ( p > 0.05 ) , although ALCA result ed in slight improvements in glucose ( 109 ± 5 to 103 ± 5 mg·dL-1 ) , HbA1c ( 6.6 ± 1.1 to 6.2 ± 1.2 % ) , and HOMA-IR ( 3.3 ± 1.3 to 2.9 ± 1.2 ) . AUC postpr and ial data were not statistically different between ALCA and placebo for any variable ( p > 0.05 ) . However , nitrate/nitrite demonstrated a moderate effect size ( r = 0.35 ) for increase from pre ( 139.50 ± 18.35 μmol·L-1·6 hr-1 ) to post ( 172.40 ± 21.75 μmol·L-1·6 hr-1 ) intervention with ALCA , and the magnitude of decrease following feeding was not as pronounced as with placebo . ConclusionS upplementation with ALCA results in an increase in resting nitrate/nitrite in pre-diabetics , without any statistically significant change in other metabolic or oxidative stress variables measured at rest or post meal Background Frailty is a biological syndrome of decreased reserve and resistance to stressors due to decline in multiple physiological systems . Amino acid deficiency , including L-carnitine , has been proposed to be associated with its pathophysiology . Nevertheless , the efficacy of L-carnitine supplementation on frailty status has not been documented . Thus , this study aim ed to determine the effect of 10-week L-carnitine supplement ( 1.5 g/day ) on frailty status and its biomarkers and also physical function , cognition , and nutritional status among prefrail older adults in Klang Valley , Malaysia . Methodology This study is a r and omized , double-blind , placebo-controlled clinical trial conducted among 50 prefrail subjects r and omized into two groups ( 26 in L-carnitine group and 24 in placebo group ) . Outcome measures include frailty status using Fried criteria and Frailty Index accumulation of deficit , selected frailty biomarkers ( interleukin-6 , tumor necrosis factor-alpha , and insulin-like growth factor-1 ) , physical function , cognitive function , nutritional status and biochemical profile . Results The results indicated that the mean scores of Frailty Index score and h and grip test were significantly improved in subjects supplemented with L-carnitine ( P<0.05 for both parameters ) as compared to no change in the placebo group . Based on Fried criteria , four subjects ( three from the L-carnitine group and one from the control group ) transited from prefrail status to robust after the intervention . Conclusion L-carnitine supplementation has a favorable effect on the functional status and fatigue in prefrail older adults The aim of the study was to evaluate the effects of 12-month treatment with sibutramine plus L-carnitine compared with sibutramine alone on body weight , glycemic control , insulin resistance , and inflammatory state in type 2 diabetes mellitus patients . Two hundred fifty-four patients with uncontrolled type 2 diabetes mellitus ( glycated hemoglobin [ HbA(1c ) ] > 8.0 % ) in therapy with different oral hypoglycemic agents or insulin  were enrolled in this study and r and omized to take sibutramine 10 mg plus L-carnitine 2 g or sibutramine 10 mg in monotherapy . We evaluated at baseline and after 3 , 6 , 9 , and 12 months these parameters : body weight , body mass index , HbA(1c ) , fasting plasma glucose , postpr and ial plasma glucose , fasting plasma insulin , homeostasis model assessment of insulin resistance index , total cholesterol , low-density lipoprotein cholesterol , high-density lipoprotein cholesterol , triglycerides , leptin , tumor necrosis factor-α , adiponectin , vaspin , and high-sensitivity C-reactive protein .  Sibutramine plus L-carnitine gave a faster improvement of fasting plasma glucose , postpr and ial plasma glucose , lipid profile , leptin , tumor necrosis factor-α , and high-sensitivity C-reactive protein compared with sibutramine alone . Furthermore , there was a better improvement of body weight , HbA(1c ) , fasting plasma insulin , homeostasis model assessment of insulin resistance index , vaspin , and adiponectin  with sibutramine plus L-carnitine compared with sibutramine alone . Sibutramine plus L-carnitine gave a better and faster improvement of all the analyzed parameters compared with sibutramine alone without giving any severe adverse effect OBJECTIVES : Nonalcoholic steatohepatitis ( NASH ) is a known metabolic disorder of the liver . No treatment has been conclusively shown to improve NASH or prevent disease progression . The function of L-carnitine to modulate lipid profile , glucose metabolism , oxidative stress , and inflammatory responses has been shown . The aim of this study was to evaluate the effects of L-carnitine 's supplementation on regression of NASH . METHODS : In patients with NASH and control subjects , we r and omly dispensed one 1-g L-carnitine tablet after breakfast plus diet and one 1 g tablet after dinner plus diet for 24 weeks or diet alone at the same dosage and regimen . We evaluated liver enzymes , lipid profile , fasting plasma glucose , C-reactive protein ( CRP ) , tumor necrosis factor (TNF)-α , homeostasis model assessment (HOMA)-IR , body mass index , and histological scores . RESULTS : At the end of the study , L-carnitine-treated patients showed significant improvements in the following parameters : aspartate aminotransferase ( P=0.000 ) , alanine aminotransferase ( ALT ) ( P=0.000 ) , γ-glutamyl-transpeptidase ( γ-GT ) ( P=0.000 ) , total cholesterol ( P=0.000 ) , low-density lipoprotein ( LDL ) ( P=0.000 ) , high-density lipoprotein ( HDL ) ( P=0.000 ) , triglycerides ( P=0.000 ) , glucose ( P=0.000 ) , HOMA-IR ( P=0.000 ) , CRP ( P=0.000 ) , TNF-α ( P=0.000 ) , and histological scores ( P=0.000 ) . CONCLUSIONS : L-carnitine supplementation to diet is useful for reducing TNF-α and CRP , and for improving liver function , glucose plasma level , lipid profile , HOMA-IR , and histological manifestations of NASH To evaluate the effects of 1-year treatment with orlistat plus L-carnitine compared to orlistat alone on body weight , glycemic and lipid control , and inflammatory parameters in obese type 2 diabetic patients . Two hundred and fifty-eight patients with uncontrolled type 2 diabetes mellitus ( T2DM ) [ glycated hemoglobin ( HbA(1c ) ) > 8.0 % ] in therapy with different oral hypoglycemic agents or insulin  were enrolled in this study and r and omized to take orlistat 120 mg three times a day plus L-carnitine 2 g one time a day or orlistat 120 mg three times a day . We evaluated the following parameters at baseline and after 3 , 6 , 9 , and 12 months : body weight , body mass index ( BMI ) , glycated hemoglobin ( HbA(1c ) ) , fasting plasma glucose ( FPG ) , postpr and ial plasma glucose ( PPG ) , fasting plasma insulin ( FPI ) , homeostasis model assessment insulin resistance index ( HOMA-IR ) , total cholesterol ( TC ) , low-density lipoprotein cholesterol ( LDL-C ) , high-density lipoprotein cholesterol ( HDL-C ) , triglycerides ( Tg ) , adiponectin ( ADN ) , leptin , tumor ne 
    Output:
    