Effects of Oral L-Carnitine Supplementation on Leptin and Adiponectin Levels and Body Weight of Hemodialysis Patients: a Randomized Clinical Trial. L-carnitine supplementation and adipokines in patients with end-stage renal disease on regular hemodialysis. Effects of supplementation with curcumin on serum adipokine concentrations: A randomized controlled trial. Potential inhibitory effects of L-carnitine supplementation on tissue advanced glycation end products in patients with hemodialysis. Effects of carnitine and coenzyme Q10 on lipid profile and serum levels of lipoprotein(a) in maintenance hemodialysis patients on statin therapy. Free and total carnitine in human serum after oral ingestion of L-carnitine. Carnitine depletion in peripheral blood mononuclear cells from patients with AIDS: effect of oral L‐carnitine A randomised, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction. Effects of L-carnitine supplementation on respiratory distress syndrome development and prognosis in premature infants: A single blind randomized controlled trial.
INTRODUCTION Carnitine supplementation may improve the general health and quality of life of hemodialysis patients by improving adipokines levels . The aim of the study was to investigate the effects of L-carnitine supplementation on leptin levels , adiponectin levels , and body weight of hemodialysis patients . MATERIAL S AND METHODS Fifty hemodialysis patients were r and omly divided into the carnitine group , who received oral L-carnitine , 1 g/L for 3 months , and the control group . Anthropometric measurements and serum levels of adipokines were measured at baseline and at the end of the intervention . RESULTS Forty-two participants completed the study . Serum leptin concentrations decreased after 12 weeks of the intervention in both groups , but these changes were not significant . The mean change of leptin concentration were , -1.7 ± 19.0 µg/mL and -7.1 ± 20.0 µg/mL in the carnitine group and the control group , respectively ( P = .39 ) . The mean adiponectin levels at baseline and after the intervention were 8.6 ± 11.19 µg/mL and 9.8 ± 4.1 µg/mL in the carnitine group ( P = .67 ) and 5.0 ± 2.5 µg/mL and 11.2 ± 5.4 µg/mL in the control group , respectively ( P < .001 ) . Serum adiponectin levels increased significantly in the control group only . The decrease in body mass index was not significant . CONCLUSIONS This study showed that a daily supplementation of 1000 mg oral syrup of L-carnitine for 12 weeks did not affect leptin and adiponectin levels or the body weight or body mass index of hemodialysis patients Chronic hemodialysis ( HD ) patients frequently encounter carnitine depletion , elevated adipose tissue-derived hormones/cytokines , that may contribute to accelerated arteriosclerosis . 10 non-diabetic HD patients were studied over 28 weeks . In the 12 weeks treatment period 1 g L-carnitine was given iv after each HD session . Measurements of plasma free- and acylcarnitines , insulin , leptin , adiponectin , resistin and ghrelin were performed at baseline , at weeks 2 , 4 , 8 , 12 ( treatment period ) and at weeks 24 - 28 ( post-treatment period ) . L-carnitine supplementation result ed in progressive increase of free- and acylcarnitine levels . Plasma levels of insulin , resistin , leptin and ghrelin remained at the already elevated baseline values . L-carnitine therapy induced a significant increase in plasma adiponectin from 20.2 ± 12.7 μg/ml ( baseline ) to 32.7 ± 20.2 μg/ml in week 2 ( p<0.05 ) and 35.4 ± 19.6 μg/ml in week 12 ( p < 0.03 ) , which remained unchanged in the post-carnitine period . Plasma insulin levels correlated positively with leptin ( r = 0.525 , p<0.0001 ) and resistin ( r = 0.284 , p<0.005 ) ; adiponectin levels correlated inversely with leptin ( r = -0.255 , p<0.02 ) and resistin ( r = -0.213 , p<0.04 ) irrespective of carnitine status . Plasma levels of adipokines and related hormones are greatly elevated in patients on regular HD  . L-carnitine administration further augmented the plasma levels of protective adiponectin , therefore it may have a role in preventing cardiovascular complications of uremia OBJECTIVE Previous experimental studies have suggested curcumin as a safe phytochemical that can improve insulin resistance through effects on adiponectin and leptin . This study aim ed to investigate the effect of curcumin on circulating adiponectin and leptin concentrations in patients with metabolic syndrome . METHODS In this pilot , r and omized , double-blind , placebo-controlled trial , subjects who met the criteria of metabolic syndrome according to the National Cholesterol Education Program Adult Treatment Panel III criteria were r and omly assigned to curcumin ( n = 59 ; 1000 mg/d ) or a placebo ( n = 58 ) for 8 wk . Serum adiponectin and leptin concentrations were determined before and after intervention . The pooled effect size for the impact of curcumin supplementation on serum adiponectin and leptin levels was also estimated using r and om-effects meta analysis . RESULTS Eight-week supplementation with curcumin was associated with a significant increase in serum adiponectin levels ( P < 0.001 ) and a reduction in serum leptin concentrations ( P < 0.001 ) . Serum leptin : adiponectin ratio was also improved by curcumin ( P < 0.001 ) . These beneficial effects of curcumin remained significant after adjustment for changes in serum lipids and glucose concentrations and baseline differences in body mass index and serum levels of glucose and glycated hemoglobin as potential confounders of treatment response . Meta analysis suggested that curcumin supplementation can increase adiponectin levels by 76.78 % ( 95 % CI : 6.14 - 147.42 ; P = 0.0330 ) , and reduce leptin by 26.49 % ( 95 % CI : -70.44 to 17.46 ) , however this latter effect size did not reach statistical significance ( P = 0.238 ) . CONCLUSIONS Curcumin can improve serum levels of adiponectin and leptin in patients with metabolic syndrome . This trial was registered at the UMIN Clinical Trials Registry ( http://www.umin.ac.jp/ctr/ ) under Trial No. UMIN000018339 BACKGROUND AND AIMS Advanced glycation end products ( AGEs ) contribute to cardiovascular disease in patients with hemodialysis ( HD ) . We have recently found that carnitine levels are inversely associated with skin AGE levels in HD patients . We examined whether L-carnitine supplementation reduced skin AGE levels in HD patients with carnitine deficiency . METHODS This was a single-center study . One hundred and two HD patients ( total carnitine levels < 50 μmol/L ) were enrolled and r and omized to either oral administration of L-carnitine ( 900 mg/day ) ( n=51 ) or control ( n=51 ) . After 6 months , metabolic and inflammatory variables , including serum levels of carnitine , were measured . Skin AGE levels were determined by evaluating skin auto-fluorescence with an AGE-reader . RESULTS There were no significant differences of clinical variables at baseline between the  control and L-carnitine therapy group . Thirty-two patients did not complete the assessment or treatment of the study .  Oral L-carnitine supplementation for 6 months significantly increased low-density lipoprotein cholesterol ( LDL-C ) , triglycerides , total , free , and acyl carnitine levels , while it decreased alanine transaminase , acyl/free carnitine ratio , β₂-microglobulin , and skin AGE values . Change in total carnitine values from baseline ( Δtotal carnitine ) and Δfree carnitine were inversely associated with Δskin AGE levels  in L-carnitine-treated patients ( p=0.036 and p=0.016 , respectively ) . In multiple regression analysis , Δfree carnitine was a sole independent determinant of Δskin AGEs ( R²=0.178 ) . CONCLUSIONS The present study demonstrated that oral L-carnitine supplementation significantly decreased skin AGE levels in HD patients with carnitine deficiency . These observations suggest that supplementation of L-carnitine might be a novel therapeutic strategy for preventing the accumulation of tissue AGEs in carnitine-deficient patients with HD INTRODUCTION Dyslipidemia and high serum lipoprotein(a ) are among the risk factors for cardiovascular diseases in hemodialysis patients .  Statins as a first line of therapy in hyperlipidemia does not always reduce the serum lipoprotein(a ) level . Several studies have reported the lipid-lowering effects of carnitine and coenzyme Q10 in hemodialysis patients . This study was design ed to investigate the effects of carnitine and coenzyme Q10 on serum lipid profile and lipoprotein(a ) level in maintenance hemodialysis patients . MATERIAL S AND METHODS This was a r and omized placebo-controlled trial . We studied on hemodialysis patients who were on treatment with atorvastatin or lovastatin to assess the efficacy of supplement therapy . They were divided into 4 groups to receive carnitine , coenzyme Q10 , both carnitine and coenzyme Q10 , and placebo . After a 3-month experiment , blood sample s were collected to measure serum levels of lipoprotein(a ) , triglyceride , total cholesterol , high-density lipoprotein cholesterol and low-density lipoprotein cholesterol . RESULTS Fifty-two hemodialysis patients , 27 men and 25 women , completed the course of the study . Three months after supplement therapy , serum levels of lipoprotein(a ) reduced significantly in the carnitine , coenzyme Q10 , and combination groups compared to the baseline values and the 3-month value of lipoprotein(a ) in the placebo group ( P = .01 ) . Serum levels of triglyceride and other lipoproteins did not significantly alter . CONCLUSIONS Our study showed that supplementation with carnitine and coenzyme Q10 could reduce serum levels of lipoprotein(a ) in maintenance hemodialysis patients treated with statins Twelve students with in apparent good health and fasting since the previous evening ingested 2 g of L-carnitine on one day and a placebo on another day in a single-blind trial . Six blood sample s were taken during the 24 h following the ingestion . Their blood carnitine levels increased ( the free form by 81 % , and the total by 57 % ) to a maximum at about 3.5 h and then slowly decreased . Twenty-four hours after ingestion , blood carnitine concentrations had still not returned to their initial levels . In the time interval where the decay curve approximated a single exponential , the half-life of the carnitine appeared to be of the order of 15 h. During the 24 h after the administration of the 2 g of L-carnitine , 7 % + /- 1 % of it was eliminated in the urine . This work suggest that the daily administration during a long period , of 2 g of L-carnitine guarantee in a healthy subject blood carnitine concentrations superior to the normal levels . Its remains to determine if the dose is sufficient in the case where L-carnitine is given to ameliorate a primary or secondary lack of carnitine , or to lower a high level of lipids in blood Objective Reduced levels of serum carnitines ( 3-hydroxy-4-N-trimethyl-ammonio-butanoate ) are found in most patients treated with zidovudine .  However , since serum carnitines do not strictly reflect cellular concentrations we examined whether a carnitine depletion could be found in peripheral blood mononuclear cells ( P BMC ) from AIDS patients with normal serum carnitine levels . In addition , we explored whether it was posssible to relate the host 's immunoreactivity to the content of carnitine in P BMC and whether carnitine levels can be corrected by oral supplementation of L-carnitine . Design Immunopharmacologic study . Methods Twenty male patients with advanced AIDS ( Centers for Disease Control and Prevention stage IVCI ) and normal serum levels of carnitines were enrolled . Patients were r and omly assigned to receive either L-carnitine ( 6g/day ) or placebo for 2 weeks . At baseline and at the end of the trial , we measured carnitines in both sera and P BMC , serum triglycerides , CD4 cell counts , and the frequency of cells entering the S and G2-M phases of cell cycle following mitogen stimulation . Results Concentrations of total carnitine in P BMC from AIDS patients was lower than in healthy controls . A significant trend towards the restoration of appropriate intracellular carnitine levels was found in patients treated with high-dose L-carnitine and was associated with an increased frequency of S and G2-M cells following mitogen stimulation . Furthermore , at the end of the trial we found a strong reduction in serum triglycerides in the L-carnitine group compared with baseline levels . Conclusions Our data indicate that carnitine deficiency occurs in P BMC from patients with advanced AIDS , despite normal serum concentrations . The increase in cellular carnitine content strongly improved lymphocyte proliferative responsiveness to mitogens . Because carnitine status is an important contributing factor to immune function in patients with advanced AIDS , we therefore believe that L-carnitine supplementation could have a role as a complementary therapy for HIV-infected individuals In a r and omised , double-blind placebo-controlled trial , the effects of the administration of oral L-carnitine ( 2 g/day ) for 28 days were compared in the management of 51 ( carnitine group ) and 50 ( placebo group ) patients with suspected acute myocardial infa rct ion . At study entry , the extent of cardiac disease , cardiac enzymes and lipid peroxides were comparable between the groups , although both groups showed an increase in cardiac enzymes and lipid peroxides . At the end of the 28-day treatment period , the mean infa rct size assessed by cardiac enzymes showed a significant reduction in the carnitine group compared to placebo . Electrocardiographic assessment of infa rct size revealed that the QRS-score was significantly less in the carnitine group compared to placebo ( 7.4 + /- 1.2 vs 10.7 + /- 2.0 ) , while serum aspartate transaminase and lipid peroxides showed significant reduction in the carnitine group . Lactate dehydrogenase measured on the sixth or seventh day following infa rct ion showed a smaller rise in the carnitine group compared to placebo . Angina pectoris ( 17.6 vs 36.0 % ) , New York Heart Association class III and IV heart failure plus left ventricular enlargement ( 23.4 vs 36.0 % ) and total arrhythmias ( 13.7 vs 28.0 % ) were significantly less in the carnitine group compared to placebo . Total cardiac events including cardiac deaths and nonfatal infa rct ion were 15.6 % in the carnitine group vs 26.0 % in the placebo group . It is possible that L-carnitine supplementation in patients with suspected acute myocardial infa rct ion may be protective against cardiac necrosis and complications during the first 28 days The aim of the present study was to investigate the efficacy of L-carnitine therapy on the occurrence and prognosis of respiratory distress syndrome ( RDS ) . A single blind , r and omized controlled trial study was conducted on 130 infants with gestational ages of 28 - 36 weeks . Infants were assigned to experimental groups ( groups 1 and 2 ) and control groups ( groups 3 and 4 ) . Groups 1 and 3 consisted of infants with RDS , and groups 2 and 4 groups were composed of infants without RDS . The experimental groups were treated with carnitine . No statistically significant differences in serum carnitine levels were detected between the study and the control groups on day 1 of treatment ( P=0.06 ) . However , on day 7 of treatment , serum carnitine levels in the experimental groups were significantly increased ( P=0.02 ) , as compared with the control groups . The surfactant requirement value , which is how many rounds of surfactant therapy were required , was 1.56±0.97 in group 1 , and 2.12±0.99 in group 3 ( P<0.001 ) . The mean duration of mechanical ventilation required was 3.04±3.60 days in group 1 , and 4.73±5.63 days in group 3 ( P<0.001 ) . The present results indicate that carnitine supplementation in premature infants with RDS may help to increase carnitine levels , thus decreasing the duration of mechanical ventilation and surfactant requirement
Conclusion l-carnitine consumption does not reduce serum leptin significantly .
However , a significant effect on leptin was observed in diabetic patients and patients who received doses more than 3 mg per day in the course of < 12 weeks
Purpose The actual effects of l-carnitine administration on leptin serum level is inconsistent .
In order to assess the efficacy of l-carnitine supplementation on serum leptin we conducted a meta- analysis of r and omized controlled trials ( RCTs ) .