Conclusion Our results indicate  that L-carnitine  reduced inflammatory mediators , especially in studies with a duration of more than 12 weeks .
Aim and background Reducing inflammation by nutritional supplements may help to reduce the risk of many chronic diseases .
Our aim in this meta- analysis was to determine the effect of L-carnitine on inflammatory mediators including C-reactive protein ( CRP ) , tumor necrosis factor-α ( TNF-α ) , and interleukin-6 ( IL-6 ) .
Effect of oral acetyl L-carnitine arginate on resting and postprandial blood biomarkers in pre-diabetics
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
Conclusion Our results indicate  that L-carnitine  reduced inflammatory mediators , especially in studies with a duration of more than 12 weeks .
Aim and background Reducing inflammation by nutritional supplements may help to reduce the risk of many chronic diseases .
Our aim in this meta- analysis was to determine the effect of L-carnitine on inflammatory mediators including C-reactive protein ( CRP ) , tumor necrosis factor-α ( TNF-α ) , and interleukin-6 ( IL-6 ) .