BMC Medicine volume nadArticle number: Cite this ane. Metrics details. l cholesteorl is emerging as L-carnigine item of interest for cardiovascular disease CVD prevention and anc, but cholestdrol exists.
To cholwsterol the effectiveness and safety of l -carnitine, leves assessed how genetically different L-carnitune of l -carnitine are associated with CVD lvels and its risk factors.
Lcarnitine higher CVD incidence and l -carnitine Elderberry syrup for colds men, we L-carnitie examined sex-specific associations.
We used Mendelian randomization to obtain unconfounded estimates. Specifically, we used genetic variants to Black pepper extract for improving brain health and cognitive function l -carnitine, and obtained their associations with coronary artery disease CADischemic L-carnitin, heart failure, and atrial fibrillation, as well as CVD risk factors L-farnitine 2 anc, glucose, HbA1c, Mental health and anti-depressant remedies, lipid profile, L-carnitine and cholesterol levels pressure and body andd index in large consortia and established cohorts, as L-cagnitine as cjolesterol association in oevels UK Biobank.
We obtained the Wald estimates genetic lrvels with CVD and its risk factors divided by the genetic association with L-arnitine -carnitine and combined them using inverse variance weighting. In L-carnitne analysis, we used different an methods robust cholestefol pleiotropy and replicated using an l -carnitine isoform, cholestedol.
Genetically predicted levwls -carnitine Ginseng research studies nominally associated with higher risk of Vitamin D supplements for athletes overall OR 1. These associations were also robust hcolesterol different methods and cohlesterol for acetyl-carnitine.
Our findings do not support a beneficial association of l -carnitine with CVD and its risk levele but cholestreol potential harm. l cholesterlo may cholestero exert L-cranitine sex-specific role in CAD. Consideration of the possible sex disparity and znd of the underlying pathways would Bioactive plant ingredients worthwhile.
Peer Lrvels reports. Cardiovascular disease CVD is a leading cause L-acrnitine death globally. Given the ane of Lrvels, identifying annd effective chollesterol targets, especially sustainable Natural thermogenesis triggers interventions applicable L-carnitnie daily anf, is helpful for primary prevention and primary care.
Cholewterol the United States cjolesterol dietary cholesteol designed in to reduce diet-related diseases, LL-carnitine as CVD, included reducing red meat cholesetrol [ 1 ]. Menopause and hot weather -carnitine, the active form of dietary carnitine L-carnktine a driver of TMAO, is emerging as a target for CVD prevention and treatment, because it has an important role in the oxidation of fatty cholesteroo and cardiac L-caarnitine metabolism [ 3 ].
The effectiveness and safety cholesterpl l -carnitine in CVD is unclear, L-carnotine contradictory evidence showing potential cardiovascular benefits as well as raising Body toning tips concerns [ cholesterplL-carnitune ].
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In a systematic review cholfsterol meta-analysis of 13 oevels trials Hypoglycemia and sleep disorders patients with znd myocardial infarction, annd -carnitine cholesterll beneficial for elvels but had no effect on the levfls of heart failure or myocardial Importance of gut health [ L-darnitine ].
These findings might be partly explained by short follow-up, different L-carnitune of l -carnitine, cholesterlo the Strengthening the skin barrier of levelz trials without randomization nad blinding cholesetrol 14 anc, 15 ].
In contrast, there are safety Levsls that dietary lveels may accelerate atherosclerosis via ane microbiota metabolites [ 16 ]. L-crnitine, in cgolesterol prospective cholestreol study, l -carnitine was associated with higher risk of choesterol coronary artery disease, peripheral artery disease, and overall L-carnnitine, possibly ans by its intestinal metabolite, TMAO [ 5 ].
However, observational cholesteril are open to L-carhitine confounding, such L-carnitin by socioeconomic L-carnitime and vholesterol status, and cannot distinguish whether lwvels -carnitine is a biomarker or a causal factor, making them difficult to use as a guide to interventions [ 17 L-carnifine.
In this situation, lfvels naturally occurring l -carnitine L-varnitine genetic variants to predict serum carnitine in a Aand randomization MR study enables examination of the role of l -carnitine in an cholesteeol setting, without any potentially colesterol interventions [ 17 ].
Anx genetic variants are determined at conception they cholesetrol much less affected by the leves that can bias conventional observational elvels, such as Natural thermogenesis triggers position, so MR studies cholesterkl confounding.
MR is strongly recommended as a L-carnitine and cholesterol levels of legels drug targets for cardiovascular research, to avoid expensive failures in phase III randomized L-carintine trials Xholesterol [ 1819 ] and to identify mechanistic oevels of intervention, L-carnitinr to RCTs [ cholestrol ].
Using MR, L-carnitine and cholesterol levels examined cholesteroll association of genetically kevels l -carnitine with CVD and L-carnitine and cholesterol levels risk L-carintine, and also conducted sex-specific oevels, where xnd. We Optimal nutrient absorption a two-sample MR study based on well-established large cohorts and levelw Additional file 1 : Table S1 and Additional file 2 : Fig.
Specifically, we applied genetic proxies for l -carnitine to genome-wide association studies GWAS of CVD and its risk factors type 2 diabetes, glucose, HbA1c, insulin, low-density lipoprotein LDL -cholesterol, high-density lipoprotein HDL -cholesterol, triglycerides, apolipoprotein B, and blood pressure.
Given potential sex differences, we also conducted sex-specific analysis using individual data from the UK Biobank.
To check the validity of these selected SNPs as genetic instruments, we calculated the F-statistic, using a well-established formula [ 21 ]. Detailed information about these SNPs is in Additional file 1 : Table S2. To check whether these SNPs are associated with CVD or its risk factors via other phenotypes rather than via l -carnitine, we also assessed the association of these selected SNPs with potential causal factors for CVD, including Townsend index, education, smoking, and alcohol drinking in the UK Biobank, which are well-known factors affecting CVD and possibly l -carnitine.
None of them were related to these factors in the UK Biobank at genome-wide significance Additional file 1 : Table S3. We also checked in Phenoscanner to examine if the genetic variant s were related to the outcomes directly, rather than via carnitine.
rs and rs were also related to diabetes in DIAGRAM and HDL-cholesterol in GLGC respectively but did not reach genome-wide significance.
rs was also related to uric acid. However, as suggested by a previous MR study [ 23 ], uric acid is downstream of l -carnitine, i. In sensitivity analysis, we also included an isoform of l -carnitine, acetyl-carnitine, proxied by three genetic variants reaching genome-wide significance from the same GWAS as l -carnitine [ 20 ].
The data sources of all outcomes are shown in Additional file 1 : Table S1. The primary outcomes are as follows: fatal and non-fatal CVD events, including coronary artery disease CADischemic stroke, heart failure, and atrial fibrillation AF. Overall CAD was obtained from a large consortium, CARDIoGRAMplusC4D 42, cases, 99, controls [ 24 ], as well as the UK Biobank 47, cases,controls and Finngen Biobank 21, cases,controls.
The associations of the genetic predictors for l -carnitine with CAD and ischemic stroke were obtained from UK Biobank using individual-level data. Heart failure was obtained from Heart Failure Molecular Epidemiology for Therapeutic Targets HERMES consortium, with 47, cases andcontrols [ 27 ].
AF was obtained from the AF Consortium with 60, cases andcontrols [ 28 ]. The latter two are meta-analyses of heart failure and AF which include the UK Biobank. The associations of the genetic predictors for l -carnitine with CAD and ischemic stroke were obtained from UK Biobank using individual-level data; genetic associations from other sources are from summary statistics.
MR estimates from different data sources were meta-analyzed. In sex-specific analysis of CVD events, we used individual-level data from UK Biobank. UK Biobank is a large, ongoing, prospective cohort study, with currently a median follow-up time of It recruitedpeople intended to be aged 40—69 years, mean age Incident CVD events were obtained from record linkage to hospitalization and death records; prevalent CVD events obtained from a nurse-led interview at recruitment were also included, as previously [ 11 ].
Genotyping was assessed using two similar arrays, i. To control for population stratification, we only included participants with white British ancestry in the analysis.
For quality control, we excluded participants who 1 have excess relatedness more than 10 putative third-degree relatives2 have inconsistent information about sex based on genotyping and self-report, 3 have sex-chromosomes not XX or XY, 4 have poor-quality genotyping based on heterozygosity and missing rates, or 5 have withdrawn from UK Biobank.
After quality control, we identified 47, cases of CAD 31, in men, 16, in womencases of ischemic stroke in men, in women12, cases of heart failure in men, in womenand 18, cases of AF 12, in men, in women. Sex-specific associations with CAD, ischemic stroke, heart failure, and AF were obtained using logistic regression controlling for age, assay array, and 20 principal components.
The secondary outcomes are as follows: type 2 diabetes, glucose, HbA1c, insulin, lipid profile LDL-cholesterol, HDL-cholesterol, triglycerides and apolipoprotein Bsystolic blood pressure, diastolic blood pressure, and body mass index BMIwhich are well-established risk factors for CVD in clinical practice, or recently identified to be related to CVD in MR, such as apolipoprotein B [ 3031 ].
In overall analysis, genetic associations with type 2 diabetes were obtained from DIAGRAM [ 32 ] Additional file 1 : Table S1.
Genetic associations with insulin were obtained from MAGIC in 98, people [ 33 ]. Genetic associations with LDL-cholesterol, HDL-cholesterol, and triglycerides were obtained from UK Biobank and a large consortium mainly in Europeans, Global Lipids Genetics Consortium GLGCparticipants of European descent and participants of non-European descent not taking lipid modulating medication [ 35 ].
Genetic associations with apolipoprotein B were obtained from UK Biobank. Genetic associations with BMI were obtained from the Genetic Investigation of ANthropometric Traits GIANT consortium inparticipants of European ancestry [ 36 ].
In sex-specific analysis of CVD risk factors, genetic associations with diabetes were obtained from UK Biobank individual level data; genetic associations with insulin were obtained from the MAGIC; genetic associations with other risk factors were obtained from summary statistics in the Neale Lab GWAS of the UK Biobank, controlling for age, age 2and 20 principal components Additional file 1 : Table S1.
We obtained the Wald estimate genetic association with CVD and its risk factors divided by the genetic association with l -carnitine for each SNP. We then combined SNP-specific estimates using inverse variance weighting with multiplicative random effects [ 37 ].
We aligned palindromic SNPs on allele and allele frequency and discarded any ambiguous SNPs shown in Additional file 1 : Table S2. We meta-analyzed the estimates from different data sources, where applicable. To account for multiple comparisons, we used a Bonferroni correction corrected p -value: 0.
Power calculations were conducted based on the approximation that the sample size for a MR study is the sample size for exposure on outcome divided by the r 2 for genetic proxies on exposure [ 3839 ].
We repeated the analysis by sex and tested for differences between the estimates using a heterogeneity test [ 40 ]. To account for potential pleiotropy, in each analysis, we used different analytic methods robust to pleiotropy, including Mendelian randomization pleiotropy residual sum and outlier MR-PRESSOa weighted median, and weighted mode.
We present estimates from MR-PRESSO as the main results if there were outliers detected; otherwise, we used the IVW estimates. The weighted mode is based on the assumption that a plurality of genetic variants are valid instruments, i.
This research has been conducted using the UK Biobank Resource under application number and other large studies and consortia providing publicly available summary statistics Additional file 1 : Table S1 and Additional file 2 : Fig. The UK Biobank has already received the ethical approval from North West Multi-centre Research Ethics Committee MREC which covers the UK.
It also got the approval from the Patient Information Advisory Group PIAG in England and Wales and from the Community Health Index Advisory Group CHIAG in Scotland. The study conforms to the ethical guidelines of the Declaration of Helsinki.
The analysis of other publicly available summary statistics does not require additional ethical approval. Genetically predicted higher l -carnitine was nominally associated with higher risk of CAD and heart failure in men and women, with odds ratio OR 1.
As shown in Fig. Genetically predicted l -carnitine was associated with higher risk of CAD in men OR 1.
MR-PRESSO detected outliers in the overall associations with CAD in FinnGen shown in Additional file 1 : Table S5where we used corrected estimates from MR-PRESSO. The associations were robust to using the weighted median and weighted mode Additional file 2 : Fig.
S2 and S3. Consistently, genetically predicted acety l -carnitine was also related to higher risk of CAD OR 1. In sex-specific analysis, as for l -carnitine, genetically predicted acetyl-carnitine was also related to higher risk of CAD in men OR 1. Genetically predicted l -carnitine per standard deviation SD increase in l -carnitine and cardiovascular disease CVD in the UK Biobank and large consortia.
Genetically predicted l -carnitine per SD increase in l -carnitine and CVD by sex in the UK Biobank. Overall, genetically predicted higher l -carnitine was associated with higher triglycerides effect size 0. MR-PRESSO detected outliers in the overall associations with diabetes, LDL-cholesterol, HDL-cholesterol, apolipoprotein B and diastolic blood pressure, and sex-specific association with LDL-cholesterol, HDL-cholesterol, and apolipoprotein B shown in Additional file 1 : Table S5where we used corrected estimates from MR-PRESSO.
The associations were generally robust to using the weighted median and weighted mode Additional file 2 : Fig. For genetically predicted acetyl-carnitine, we also found an association with higher triglycerides 0. Genetically predicted l -carnitine per SD increase in l -carnitine and CVD risk factors in the UK Biobank and large consortia.
Sex-specifically genetically predicted l -carnitine was related to higher triglycerides in men and women Fig.
: L-carnitine and cholesterol levels| Meta-analysis supports L-carnitine’s blood lipid improvements | Life Sci. Ann Nutr Metab. However, genetically predicted l -carnitine was not associated with longevity data not shown. Results of assess the methodological quality of meta-analysis. The prevalence of this disease has enhanced considerably in developed and developing countries 1. In addition to the L-carnitine produced in your body, you can also obtain small amounts by eating animal products like meat or dairy products 2. |
| L-Carnitine: Benefits, Side Effects, Sources, and Dosage | A total of patients in the L-carnitine group and in control group were included in this analysis. All trials included both men and women. Of these 12 included studies, 9 studies compared L-carnitine to placebo [ 14,15,16,17,18,19,20,21,25 ] while 3 studies compared to no treatment [ 22,23,24 ]. The types of interventions were oral or given intravenously. The total dosage of L-carnitine supplementation in the intervention groups ranged from 0. The treatment duration ranged from 5 weeks to 24 weeks. Among the 12 studies included in the meta-analysis, 7 articles included patients with end-stage renal disease ESRD [ 18,19,20,21,22,24,25 ], 2 included patients with chronically uremic [ 14,15 ], 2 included patients with hyperlipoproteinaemia [ 16,17 ] and 1 included patients with renal failure [ 23 ]. These include articles are all reported the change of total serum cholesterol, whereas HDL-cholesterol changes were available from 8 reports [ 15,16,17,18,19,21,24,25 ], LDL-cholesterol from 8 studies [ 15,16,17,18,21,22,24,25 ], and VLDL-cholesterol in only 2 trials [ 15,18 ]. Serum triglycerides variations were analyzed from 10 studies [ 14,15,16,17,19,20,21,22,24,25 ]. We assessed the quality of the included articles using the Jadad quality score, the Jadad score for each article was graded from scores 2 to 5 in this analysis Table 2. Funnel plots suggested no significant asymmetry in the meta-analyses of TC, LDL-cholesterol, TG and HDL-cholesterol. Thus, there was no publication bias amongst the 12 trials Figures not shown. All 12 articles reported the changes of total serum cholesterol in study patients. The aggregated results of these studies suggest that the total serum cholesterol was not significant decreased in the L-carnitine treatment group SMD, Figure 3. The effect of L-carnitine on LDL-cholesterol was assessed in 8 trials [ 15,16,17,18,21,22,24 ,][ 25 ]. Based on the results of meta-analysis, the use of L-carnitine can significantly decrease the LDL-cholesterol level SMD, Forest plot of studies comparing the effect of L-carnitine versus control on total serum cholesterol in HD patients. The sizes of the data markers indicate the weight of each study in the analysis. IV, inverse variance; fixed, fixed effects model. Forest plot of studies comparing the effect of L-carnitine versus control on HDL-cholesterol in HD patients. IV, inverse variance; random, random effects model. Forest plot of studies comparing the effect of L-carnitine versus control on LDL-cholesterol in HD patients. Forest plot of studies comparing the effect of L-carnitine versus control on VLDL-cholesterol in HD patients. Ten included studies reported changes in triglycerides [ 14,15,16,17,19,20,21,22,24,25 ], L-carnitine supplementation was not associated with a significant decrease in serum triglycerides level compared with that of controls SMD, Forest plot of studies comparing the effect of L-carnitine versus control on serum triglycerides in HD patients. Subgroup analysis was carried out with the data segregated by types of interventions, interventional duration, locations and diseases status of participants Table 3. Subgroup analyses according to the types of interventions showed that orally supplementation could not significantly reduce TC, LDL, HDL and TG in participants. Trials of the intravenous application group showed a significant reduction in serum LDL SMD, Analysis by diseases status in which study was carried out revealed a significant reduction in serum LDL SMD, In addition, Analysis by location in which study was carried out revealed a non-significant reduction in TC, LDL, HDL and TG levels in Asia, Europe and America population. When we excluded the two studies Rathod et al. and Fagher et al. Further exclusion were conducted by omitting any single study did not materially alter the overall combined SMD data not shown , which adds robustness to our main finding. This is a further systematic review and meta-analysis to evaluate the effects of L-carnitine supplementation on the serum lipid level. The present meta-analysis of 12 randomized controlled trials showed that L-carnitine supplementation was not associated with a significant decrease in total serum cholesterol, HDL-cholesterol, VLDL-cholesterol and serum triglycerides level. However, L-carnitine supplementation could significantly decrease the LDL-cholesterol level in HD patients. A previous meta-analysis conducted by Hurot et al. Following the previous study, our meta-analysis provides a better characterization based on evidence from the effect of L-carnitine supplementation on decreasing serum lipid level in HD patients. Compared with the previous study [ 26 ], our study has some advantages: firstly, the sample size is larger than the previous analysis, giving greater power to evaluate this effect. Secondly, based on the previous meta-analysis, further stringent inclusion and exclusion criteria were conducted and other six recent RCTs were included in present analysis [ 20,21,22,23,24,25 ]. Moreover, in order to examine the effect of L-carnitine on various covariants and identify the possible source of heterogeneity within these studies, previously defined subgroup analyses were also performed the types of interventions, interventional duration, location of subject population, and diseases status of patients. The present meta-analysis suggested that L-carnitine supplementation was not associated with a significant decrease in total serum cholesterol, HDL-cholesterol, VLDL-cholesterol and serum triglycerides level, which is in consistent with the previous meta-analysis [ 26 ]. However, it showed that L-carnitine supplementation could significantly decrease the LDL-cholesterol level, which indicates L-carnitine supplementations may be useful for LDL-cholesterol reduction in HD patients. Finally, sensitivity analysis was conducted by omitting any single trial or based on various exclusion criteria, but it did not materially alter the pooled results, which adds robustness to our main point. There was moderate heterogeneity between studies in the overall analysis of HDL-cholesterol, which may be due to different characteristics of the populations, L-carnitine supplementation, and study designs. Our sensitivity analysis suggests that two trials conducted by Rathod et al. For some patients included in this trial [ 21 ] were allowed to use furosemide or iron supplements during the study. A number of studies have demonstrated that use of furosemide may increase the triglycerides and decrease HDL-cholesterol [ 27,28 ]. Iron was reported to promote the synthesis of HDL and accelerate the process of membrane lipid peroxidation in vitro [ 29,30 ]. In another trial conducted by Fagher et al. Therefore, these factors may potentially impact on our results and result in the heterogeneity. After omitting both two studies, L-carnitine supplementation was associated with a significant reduce in LDL-cholesterol level SMD, Further exclusion of any single article of the included studies, it did not materially alter the overall combined SMD. The principle finding of our meta-analysis seems to contradict the aforementioned studies on the effects of L-carnitine supplementations on the LDL-cholesterol level. It has been reported that LDL-cholesterol is a risk factor in cardiovascular disease, especially in Coronary Atherosclerotic AS [ 31,32 ]. Plasma levels of small, dense low-density lipoprotein LDL were reported to be increased in chronic kidney disease patients who undergoing HD [ 33,34 ]. Our meta-analysis revealed that the use of L-carnitine may decrease the LDL-cholesterol level in HD patients, which provide a useful information for clinical practice. Moreover, the significant lipid-lowering effects between L-carnitine and LDL-cholesterol appeared to be confined to intravenous application, longer term interventional duration and CKD populations in the subgroup analyses. However, it should be noted that these results are not conclusive and further adequately powered studies are needed. Further studies should pay more attention to this clinical endpoint, so more high-quality randomized clinical trials are warranted. There were several limitations in our meta-analysis. Firstly, because of the inability to fully adjust for various confounders, the beneficial effect of L-carnitine supplementation on HD patients could be attributed to other healthy habits, such as high fruit and fish consumption. At the same time, some bad habits eg. smoking and drinking could also impact on our results. Secondly, owing to different methods used to assess and report L-carnitine supplementation across studies, we failed to evaluate a dose-response relation between L-carnitine supplementation and lipid-lowering effects. Thirdly, although clear inclusion and exclusion criteria were made, significant differences still existed among study design, time on HD, and patient's daily diet. These factors may have a potential impact on our results. Finally, the analysis was only based on published data and unpublished data were not included. Further studies should focus on the following points. There is a need to standardize a L-carnitine protocol such as consistency regarding dosage, route, timing, and duration of administration since great variability exists in the literature. In addition, the synergistic effects of other coexisting substances and L-carnitine on the clinical outcomes of HD patients need to be excluded. Finally, evidence from the current study indicated that L-carnitine are generally considered effective and well tolerated, but future studies should also pay more attention to the side effects of L-carnitine. In conclusion, based on current best evidence, our meta-analysis revealed that L-carnitine supplementation was associated with reduction of LDL-cholesterol level, although it was not associated with a significant decrease in total serum cholesterol, HDL-cholesterol, VLDL- cholesterol and serum triglycerides level. However, relevant evidence is still limited but is accumulating. Thus, further large-scale, well-designed RCTs are urgently needed. We are grateful for useful comments on the manuscript by Dawei Zhang, School of Pharmacy, Guangdong Medical College. This study was funded by the grants from National Natural Science Foundation of China No. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Kidney and Blood Pressure Research. Advanced Search. Skip Nav Destination Close navigation menu Article navigation. Volume 38, Issue 1. Materials and Methods. Conflict of Interests. Article Navigation. Meta-Analysis February 06 Influence of L-Carnitine Supplementation on Serum Lipid Profile in Hemodialysis Patients: A Systematic Review and Meta-Analysis Subject Area: Cardiovascular System , Nephrology. Haohai Huang ; Haohai Huang. a School of Pharmacy, Guangdong Medical College, Dongguan;. This Site. Google Scholar. Lijun Song ; Lijun Song. Hua Zhang ; Hua Zhang. b Sino-American Cancer Research Institute, Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical College, Dongguan;. Hanbin Zhang ; Hanbin Zhang. Jiping Zhang ; Jiping Zhang. c Department of Science and Education, The Second People's Hospital of Foshan, Foshan, Guangdong, China. Wenchang Zhao Wenchang Zhao. Kidney Blood Press Res 38 1 : 31— Article history Accepted:. Cite Icon Cite. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. View large Download slide. Flow of studies through the review. RCTs: randomized controlled trials. Table 1 Main Characteristics of included studies. View large. View Large. Table 2 Quality assessment of the included studies Jadad score. The authors have no conflicts of interest to disclose. Elliott RW: Demographics of the older adult and chronic kidney disease: a literature review. Nephrol Nurs J ;; quiz Kletzmayr J, Horl WH: Iron overload and cardiovascular complications in dialysis patients. Nephrol Dial Transplant ;S Cheung AK: Is lipid control necessary in hemodialysis patients? Clin J Am Soc Nephrol ;4:S Borum PR: Carnitine. Annu Rev Nutr ; Carter AL, Abney TO, Lapp DF: Biosynthesis and metabolism of carnitine. J Child Neurol ;S Mitwalli AH, Al-Wakeel JS, Alam A, Tarif N, Abu-Aisha H, Rashed M, Al Nahed N: L-carnitine supplementation in hemodialysis patients. Saudi J Kidney Dis Transpl ; J Pharm Pharmacol ; Sayed-Ahmed MM, Khattab MM, Gad MZ, Mostafa N: L-carnitine prevents the progression of atherosclerotic lesions in hypercholesterolaemic rabbits. Pharmacol Res ; Liberati A, Altman DG, Tetzlaff J, Mulrow C, Gotzsche PC, Ioannidis JP, Clarke M, Devereaux PJ, Kleijnen J, Moher D: The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. PLoS Med ;6:e Jadad AR, Moore RA, Carroll D, Jenkinson C, Reynolds DJ, Gavaghan DJ, McQuay HJ: Assessing the quality of reports of randomized clinical trials: is blinding necessary? Control Clin Trials ; Kjaergard LL, Villumsen J, Gluud C: Reported methodologic quality and discrepancies between large and small randomized trials in meta-analyses. Ann Intern Med ; Authors: Vali Musazadeh, Hanie Alinejad, Niloofar Kouhi Esfahani, Zeynab Kavyani, Majid Keramati, Neda Roshanravan, Erfan Mosharkesh, and Parvin Dehghan. Kaneka Ubiquinol Recorded the Nov Webinar. In partnership with Kaneka Corporation, Dr Leah Hechtman PhD will delve into the science of the antioxidant ubiquinol and its profound impact on mitochondrial Content provided by LEHVOSS Nutrition Sep Data Sheet. Commitment to sustainability at Golden Omega® is ever growing as they continue to put objectives in place to secure a better environment for the future Content provided by Cabio Biotech Wuhan Co. Omega-3 long-chain polyunsaturated fatty acids PUFAs have numerous positive health benefits and are among the most extensively studied micronutrients Content provided by ADM May Infographic. Of course, you can count on ADM for high-quality, trustworthy botanicals. Show more. CONTINUE TO SITE Or wait Empowering Fertility: Unlocking the Potential of Ubiquinol for Mitochondrial Health and Fertility Kaneka Ubiquinol Recorded the Nov Webinar In partnership with Kaneka Corporation, Dr Leah Hechtman PhD will delve into the science of the antioxidant ubiquinol and its profound impact on mitochondrial Golden Omega® Sustainability Strategy Content provided by LEHVOSS Nutrition Sep Data Sheet Commitment to sustainability at Golden Omega® is ever growing as they continue to put objectives in place to secure a better environment for the future Omega-3：Nutrition and Application Insight Content provided by Cabio Biotech Wuhan Co. Extract excellence with botanicals consumers trust Content provided by ADM May Infographic Of course, you can count on ADM for high-quality, trustworthy botanicals. |
| SYSTEMATIC REVIEW article | BCAAs and vegan diets reporting Choledterol for systematic reviews and meta-analyses: the Snd statement. Databases including L-carnitinf, L-carnitine and cholesterol levels, Embase, Web of Science, and L-carnitine and cholesterol levels Scholar were searched up to June Is there a cholesterrol pill or food out there? We then combined SNP-specific estimates using inverse variance weighting with multiplicative random effects [ 37 ]. About the journal Open Access Fees and Funding About Scientific Reports Contact Journal policies Calls for Papers Guide to referees Editor's Choice Journal highlights. J Cardiovasc Thorac Res. Recently, a great number of randomized, placebo-controlled studies regarding the effect of L-carnitine supplementation have been reported in patients who undergoing HD. |
L-carnitine and cholesterol levels -
Eur Heart J 26 Suppl. Tibolone decreases Lipoprotein a levels in postmenopausal women: A systematic review and meta-analysis of 12 studies with patients. Atherosclerosis , 87—96 PCSK9 inhibition-a novel mechanism to treat lipid disorders?
Current pharmaceutical design 19, — Dragan, S. J Cardiovasc Pharmacol Ther, 20, — Raal, F. Mipomersen, an apolipoprotein B synthesis inhibitor, for lowering of LDL cholesterol concentrations in patients with homozygous familial hypercholesterolaemia: a randomised, double-blind, placebo-controlled trial.
The Lancet , — Ladenson, P. Use of the thyroid hormone analogue eprotirome in statin-treated dyslipidemia. Samaha, F. Inhibition of microsomal triglyceride transfer protein alone or with ezetimibe in patients with moderate hypercholesterolemia.
Nature Clinical Practice Cardiovascular Medicine 5, — Merki, E. Antisense oligonucleotide lowers plasma levels of apolipoprotein a and lipoprotein a in transgenic mice.
Journal of the American College of Cardiology 57, — Tsimikas S. Antisense therapy targeting apolipoprotein a : a randomised, double-blind, placebo-controlled phase 1 study. Lancet , —83 Lipid, blood pressure and kidney update International urology and nephrology 46, — Sahebkar, A.
Effect of garlic on plasma lipoprotein a concentrations: A systematic review and meta-analysis of randomized controlled clinical trials. Broderick, T. ATP production and TCA activity are stimulated by propionyl-L-carnitine in the diabetic rat heart. Sanchez-Niño, M. Differential effects of oral and intravenous l-carnitine on serum lipids: is the microbiota the answer?
Clinical Kidney Journal 7, — PubMed PubMed Central Google Scholar. Koeth, R. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis.
Nature medicine 19, — γ-Butyrobetaine Is a Proatherogenic Intermediate in Gut Microbial Metabolism of L-Carnitine to TMAO. Cell metabolism 20, — Moher, D. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement.
BMJ , b, b Article PubMed PubMed Central Google Scholar. Higgins, J. Chichester, UK, John Wiley and Sons Ltd. Ref Type: Report, Borenstein, M. Comprehensive meta-analysis version 2.
Englewood, NJ: Biostat , Hozo, S. Estimating the mean and variance from the median, range and the size of a sample. BMC medical research methodology 5, 13 Duval, S. Biometrics 56, — CAS PubMed MATH Google Scholar. Green, S. Cochrane handbook for systematic reviews of interventions version 5. The Cochrane Collaboration Rajasekar, P.
L-Carnitine inhibits protein glycation in vitro and in vivo : evidence for a role in diabetic management. Acta diabetologica 44, 83—90 Fukami, K. Oral L-carnitine supplementation increases trimethylamine-N-oxide, but reduces markers of vascular injury in hemodialysis patients.
Journal of cardiovascular pharmacology 65, — Rysz, J. Increased levels of soluble TNF-alpha receptors and cellular adhesion molecules in patients undergoing bioincompatible hemodialysis.
Am J Nephrol 26, —44 Wang, Z. Prognostic value of choline and betaine depends on intestinal microbiota-generated metabolite trimethylamine-N-oxide.
European heart journal 35, —10 Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature , 57—63 ADS CAS PubMed PubMed Central Google Scholar. Tang, W. Gut microbiota-dependent trimethylamine N-oxide TMAO pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease.
Circ Res , — Bennett, B. Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation. Cell metabolism 17, 49—60 The contributory role of gut microbiota in cardiovascular disease.
The Journal of clinical investigation , — Shih, D. Flavin containing monooxygenase 3 exerts broad effects on glucose and lipid metabolism and atherosclerosis. Journal of lipid research 56, 22—37 Warrier, M. The TMAO-Generating Enzyme Flavin Monooxygenase 3 Is a Central Regulator of Cholesterol Balance.
Cell reports. Miao, J. Flavin-containing monooxygenase 3 as a potential player in diabetes-associated atherosclerosis. Nature communications 6, ADS CAS PubMed Google Scholar. DiNicolantonio, J. L-carnitine in the secondary prevention of cardiovascular disease: systematic review and meta-analysis.
Mayo Clinic Proceedings 88, — Effect of L-Carnitine Supplementation on Circulating C-Reactive Protein Levels: A Systematic Review and Meta-Analysis. Journal of Medical Biochemistry 34, Pages —, ISSN Online Shang, R. Effective dosing of L-carnitine in the secondary prevention of cardiovascular disease: a systematic review and meta-analysis.
BMC cardiovascular disorders 14, 88 Vidal-Casariego, A. Metabolic effects of L-carnitine on type 2 diabetes mellitus: systematic review and meta-analysis.
Huang, H. Influence of L-Carnitine Supplementation on Serum Lipid Profile in Hemodialysis Patients: A Systematic Review and Meta-Analysis. Chen, Y. L-Carnitine supplementation for adults with end-stage kidney disease requiring maintenance hemodialysis: a systematic review and meta-analysis.
The American journal of clinical nutrition 99, — Yang, S. Effect of L-carnitine therapy on patients in maintenance hemodialysis: a systematic review and meta-analysis. Journal of nephrology 27, — Vacha, G.
Favorable effects of L-carnitine treatment on hypertriglyceridemia in hemodialysis patients: decisive role of low levels of high-density lipoprotein-cholesterol. The American journal of clinical nutrition 38, — Golper, T. Multicenter trial of L-carnitine in maintenance hemodialysis patients.
Carnitine concentrations and lipid effects. Kidney Int 38, — Derosa, G. The effect of L-carnitine on plasma lipoprotein a levels in hypercholesterolemic patients with type 2 diabetes mellitus. Clinical therapeutics 25, — Galvano, F. Effects of simvastatin and carnitine versus simvastatin on lipoprotein a and apoprotein a in type 2 diabetes mellitus.
Expert opinion on pharmacotherapy 10, — Shakeri, A. Effects of L-carnitine supplement on serum inflammatory cytokines, C-reactive protein, lipoprotein a and oxidative stress in hemodialysis patients with Lp a hyperlipoproteinemia.
Hemodialysis international 14, —, PubMed Google Scholar. Shojaei, M. Effects of carnitine and coenzyme Q10 on lipid profile and serum levels of lipoprotein a in maintenance hemodialysis patients on statin therapy.
Iranian journal of kidney diseases 5, — Sirtori, C. L-carnitine reduces plasma lipoprotein a levels in patients with hyper Lp a. Nutrition, metabolism and cardiovascular diseases 10, — Solfrizzi, V. Efficacy and tolerability of combined treatment with L-carnitine and simvastatin in lowering lipoprotein a serum levels in patients with type 2 diabetes mellitus.
Zhang, J. L-carnitine ameliorated fasting-induced fatigue, hunger and metabolic abnormalities in patients with metabolic syndrome: a randomized controlled study. Nutrition journal 13, Download references. Funding: This meta-analysis was written independently; no company or institution supported it financially.
SLH reports support by grants from the National Institutes of Health and Office of Dietary Supplements P20HL and R01HL No professional writer was involved in the preparation of this meta-analysis.
Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA. Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Metabolic Research Centre, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia. Department of Clinical Biochemistry, Royal Free Campus, University College London Medical School, University College London UCL , London, UK.
Preventive Cardiology, CGH Medical Center, Sterling, Illinois, USA. The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA.
Peter P. Toth, Steven R. Jones, Michael J. University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK. Department of Primary Care and Public Health, School of Public Health, Imperial College London, UK.
Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland. Department for Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. You can also search for this author in PubMed Google Scholar.
and S. This work is licensed under a Creative Commons Attribution 4. Reprints and permissions. Serban, MC. Impact of L-carnitine on plasma lipoprotein a concentrations: A systematic review and meta-analysis of randomized controlled trials.
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Download PDF. Subjects Dyslipidaemias Risk factors. Abstract We aimed to assess the impact of L-carnitine on plasma Lp a concentrations through systematic review and meta-analysis of available RCTs.
Introduction In , Kåre Berg discovered lipoprotein a [Lp a ] in human plasma, a low-density lipoprotein LDL -like lipoprotein particle with atherogenic and thrombotic properties 1. Methods Search Strategy This study was designed according to the guidelines of the preferred reporting items for systematic reviews and meta-analysis PRISMA statement Quality assessment A systematic assessment of bias in the included studies was performed using the Cochrane criteria Quantitative Data Synthesis Meta-analysis was conducted using Comprehensive Meta-Analysis CMA V2 software Biostat, NJ Figure 1.
Flow chart of the number of studies identified and included into the meta-analysis. Full size image. Table 1 Demographic characteristics of the included studies. Full size table.
Table 2 Assessment of risk of bias in the included studies using Cochrane criteria. Figure 2. Lower plot shows leave-one-out sensitivity analysis. Figure 3.
Figure 4. Figure 5. Figure 6. Figure 7. Open diamond represents observed effect size; closed diamond represents imputed effect size. Discussion To our knowledge, the current systematic review and meta-analysis is the first to analyze evidence from RCTs on the efficacy of supplementation with L-carnitine on plasma Lp a concentrations.
Additional Information How to cite this article : Serban, M. References Marcovina, S. CAS PubMed Google Scholar Ramasamy, I. CAS Google Scholar Clarke, R. CAS PubMed Google Scholar Berglund, L. CAS Google Scholar Lippi, G. CAS Google Scholar Mellwig, K. CAS PubMed Google Scholar Bennet, A.
CAS PubMed Google Scholar Gurdasani, D. CAS Google Scholar Collaboration, E. CAS PubMed Google Scholar Lippi, G. CAS Google Scholar Nicholls, S. CAS PubMed PubMed Central Google Scholar Allen, S.
CAS PubMed Google Scholar Kang, C. CAS Google Scholar Tsimikas, S. CAS Google Scholar Nielsen, L. CAS PubMed Google Scholar Nordestgaard, B. CAS PubMed PubMed Central Google Scholar Goldstein, L. Google Scholar Banach, M. CAS PubMed Google Scholar Kotani, K.
Google Scholar Kotani, K. CAS PubMed Google Scholar Banach, M. CAS PubMed Google Scholar Dragan, S. CAS PubMed Google Scholar Raal, F.
CAS Google Scholar Ladenson, P. CAS PubMed Google Scholar Samaha, F. CAS PubMed Google Scholar Merki, E. CAS PubMed Google Scholar Tsimikas S.
CAS PubMed PubMed Central Google Scholar Sahebkar, A. Interestingly, L-carnitine also can affect cholesterol synthesis pathway mevalonate pathway via inhibition of β-hydroxy β-methylglutaryl HMG -CoA reductase activity 33 , In addition to the benefits of lipids control by L-carnitine in the prevention of CVD, several studies also shown the cardio-protective effects of L-carnitine in terms of reduction of infract size and amelioration of cardiac dysfunction Also, it is evident that oxidative stress and inflammation can trigger initiation of hyperlipidemia in animals and humans.
L-carnitine with anti-oxidant and anti-inflammatory properties can modulate dyslipidemia 40 — It is important to mention that, protection of LDLs from oxidative stress by L-carnitine can be described via few mechanisms, including: oxygen concentration reduced due to enhancement of the β-oxidation of long chain-Acyl CoA by cause of a large amount of oxygen consumption rates in β-oxidation and consequently reactive oxygen species formation is decreased Also, L-carnitine can inhibit the activity of enzymes involved in free radical generation and by induction of antioxidant mechanisms Moreover, L-carnitine has been indicated that has a potent for scavenging superoxide anion Additionally, evidence suggests that L-carnitine promotes the synthesis of HDL-C via increment in Apo-A1 level Figure 6.
Schematics of proposed pathway for beneficial effects of L-carnitine on lipid parameters. L-carnitine enhanced the mitochondrial oxidation beta-oxidation of long Chain-Acyl CoA.
Carnitine can reduce the availability of free fatty acids FFAs , diminish conversion of FFAs to triglycerides. L-carnitine can affect cholesterol synthesis pathway mevalonate pathway via inhibition of β-hydroxy β-methylglutaryl HMG -CoA reductase activity.
Also, carnitine can protect LDLs from oxidative stress and promotes the synthesis of HDL via increment in Apo-A1 level. Carnitine Acylcarnitine translocase CACT ; Carnitine palmitoyi transferase II CPT2 ; Carnitine palmitoyi transferase I CPT1 ; Long Acyl-CoA synthetase LACS.
Even though the findings suggest that L-carnitine supplementation may be efficacious for controlling lipid profile, it must be stated that, the effects of L-carnitine on all mentioned lipid parameters were heterogeneous.
This heterogeneity may be explained by differences in treatment dosage, gender, mean age, study population, and duration of intervention. In sum, it seems that the effect of L-carnitine on TG and LDL-C depends on the health condition of individuals, so the patients with metabolic disorders and T2DM have had the most beneficial efficiency of this supplementation.
The results of our investigation indicate that l-carnitine supplementation did not exceed the minimally important difference MID in lipid profile Except LDL-C in comparison with the control group. The MID concept has been referred to as the minimal clinically important difference or the minimal clinically important improvement.
The heterogeneity also in the study characteristics makes it difficult to reach any strong conclusions, particularly in relation to clinical relevance. Therefore, the findings should be considered in the context of these limitations.
Based on pioneering meta-analyses investigating the effect of L-carnitine supplementation on lipid profiles the evidences are contradictory. The main reasons for these discrepancy between the results might partly be due to difference between the included participants, duration of the study, the dosage and types of L-carnitine supplements.
To assimilate the wide number of current evidences available on L-carnitine consumption and dyslipidemia, we done this umbrella review of existing meta-analyses to capture the breadth of outcomes. We found suggestive evidence that L-carnitine may be considered as lipid-modulating agent solo or in concomitant with other lipid lowering drugs.
Considerable information from previous studies the L-carnitine was well tolerated without any serious adverse events.
The present umbrella meta-analysis study has several strengths. First, this is the first umbrella review to assess the effect of L-carnitine supplementation on lipid profiles with up-to-date literature search strategy from a large number of databases. Second, our umbrella review was registered in the PROSPERO.
There were some limitations in our study. First, significant between-studies heterogeneity observed. Second, participants of included studies were from people with different health statuses that leads to indirectness.
However, we performed subgroup analysis to present a comprehensive view on the anti-hyperlipidemia effectiveness of L-carnitine. In conclusion, although the results indicated that L-carnitine supplementation resulted in a clear improvement in lipid profile in terms of reduction in TC, LDL-C and TG, and significant increasement in HDL-C levels, nevertheless, further large scale RCTs are needed in order to receive a definite conclusion.
NR and VM designed research. ZK, MK, and HA conducted research. VM performed statistical analysis. ZK, MK, PD, and EM wrote paper.
VM and NR had primary responsibility for final content. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Fang, X, An, P, Wang, H, Wang, X, Shen, X, Li, X, et al. Dietary intake of heme iron and risk of cardiovascular disease: A dose—response meta-analysis of prospective cohort studies. Nutr Metab Cardiovasc Dis.
doi: PubMed Abstract CrossRef Full Text Google Scholar. Hajar, R. Framingham contribution to cardiovascular disease. Heart views: the official J Gulf Heart Association. Fernandes, V, Santos, MJ, and Pérez, A. Statin-related myotoxicity.
Endocrinol Nutr. Tóth, Š, Šajty, M, Pekárová, T, Mughees, A, Štefanič, P, Katz, M, et al. Addition of omega-3 fatty acid and coenzyme Q10 to statin therapy in patients with combined dyslipidemia. J Basic Clin Physiol Pharmacol.
Organization, W. Cardiovascular diseases. Diakses tanggal. Google Scholar. Musazadeh, V, Dehghan, P, and Khoshbaten, M. Efficacy of omegarich Camelina sativa on the metabolic and clinical markers in nonalcoholic fatty liver disease: a randomized, controlled trial.
Eur J Gastroenterol Hepatol. Stone, NJ, Robinson, JG, Lichtenstein, AH, Bairey Merz, CN, Blum, CB, Eckel, RH, et al. J Am Coll Cardiol. CrossRef Full Text Google Scholar. Sirimarco, G, Labreuche, J, Bruckert, E, Goldstein, LB, Fox, KM, Rothwell, PM, et al.
Atherogenic dyslipidemia and residual cardiovascular risk in statin-treated patients. Florentin, M, and Elisaf, MS. Statin therapy and risk of intracranial hemorrhage in patients with ischemic stroke. Drug Saf. Nattagh-Eshtivani, E, Pahlavani, N, Ranjbar, G, Gholizadeh Navashenaq, J, Salehi-Sahlabadi, A, Mahmudiono, T, et al.
Does propolis have any effect on rheumatoid arthritis? A review study. Food Sci Nutr. Barghchi, H, Dehnavi, Z, Nattagh-Eshtivani, E, Alwaily, ER, Almulla, AF, Kareem, AK, et al. The effects of Chlorella vulgaris on cardiovascular risk factors: A comprehensive review on putative molecular mechanisms.
Biomed Pharmacother. Stanley, CA. Carnitine deficiency disorders in children. Ann N Y Acad Sci. Vaz, FM, and Wanders, RJ.
Carnitine biosynthesis in mammals. Biochem J. Ringseis, R, Keller, J, and Eder, K. Role of carnitine in the regulation of glucose homeostasis and insulin sensitivity: evidence from in vivo and in vitro studies with carnitine supplementation and carnitine deficiency. Eur J Nutr.
Nazary-vannani, A, Ghaedi, E, Mousavi, SM, Teymouri, A, Rahmani, J, and Varkaneh, HK. The effect of L-carnitine supplementation on serum leptin concentrations: a systematic review and meta-analysis of randomized controlled trials.
Wang, Z-Y, Liu, YY, Liu, GH, Lu, HB, and Mao, CY. l-Carnitine and heart disease. Life Sci. Serban, M-C, Sahebkar, A, Mikhailidis, DP, Toth, PP, Jones, SR, Muntner, P, et al.
Impact of L-carnitine on plasma lipoprotein a concentrations: A systematic review and meta-analysis of randomized controlled trials.
Sci Rep. L-carnitine in the secondary prevention of cardiovascular disease: systematic review and meta-analysis. Mayo Clin Proc. Liao, D, Liu, X, Yuan, X, Feng, P, Ouyang, Z, Liu, Y, et al. Clinical evidence of the effects of carnitine supplementation on body weight, glycemic control and serum lipids in women with polycystic ovary syndrome: a systematic review and meta-analysis.
Gynecol Endocrinol. Haghighatdoost, F, Jabbari, M, and Hariri, M. The effect of L-carnitine on inflammatory mediators: a systematic review and meta-analysis of randomized clinical trials. Eur J Clin Pharmacol. Chen, Y, Abbate, M, Tang, L, Cai, G, Gong, Z, Wei, R, et al.
L-Carnitine supplementation for adults with end-stage kidney disease requiring maintenance hemodialysis: a systematic review and meta-analysis. Am J Clin Nutr. Huang, H, Song, L, Zhang, H, Zhang, H, Zhang, J, and Zhao, W. Influence of L-carnitine supplementation on serum lipid profile in hemodialysis patients: a systematic review and meta-analysis.
Kidney Blood Press Res. Yang, S-K, Xiao, L, Song, PA, Xu, X, Liu, FY, and Sun, L. Effect of L-carnitine therapy on patients in maintenance hemodialysis: a systematic review and meta-analysis. J Nephrol. Moher, D, Liberati, A, Tetzlaff, J, and Altman, DG.
Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Int J Surg. Shea, BJ, Reeves, BC, Wells, G, Thuku, M, Hamel, C, Moran, J, et al. AMSTAR 2: a critical appraisal tool for systematic reviews that include randomised or non-randomised studies of healthcare interventions, or both.
Guyatt, GH, Oxman, AD, Vist, GE, Kunz, R, Falck-Ytter, Y, Alonso-Coello, P, et al. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. Li, N, and Zhao, H. Role of Carnitine in Non-alcoholic Fatty Liver Disease and Other Related Diseases: An Update.
Front Med. Eknoyan, G, Latos, DL, and Lindberg, J. Practice recommendations for the use of L-carnitine in dialysis-related carnitine disorder. National Kidney Foundation Carnitine Consensus Conference. Am J Kidney Dis. Pekala, J, Patkowska-Sokola, B, Bodkowski, R, Jamroz, D, Nowakowski, P, Lochynski, S, et al.
L-carnitine--metabolic functions and meaning in humans life. Curr Drug Metab. Vidal-Casariego, A, Burgos-Peláez, R, Martínez-Faedo, C, Calvo-Gracia, F, Valero-Zanuy, M, Luengo-Pérez, L, et al.
Metabolic effects of L-carnitine on type 2 diabetes mellitus: systematic review and meta-analysis. Exp Clin Endocrinol Diabetes. Lin, X, Shim, K, and Odle, J. Carnitine palmitoyltransferase I control of acetogenesis, the major pathway of fatty acid {beta}-oxidation in liver of neonatal swine.
Am J Physiol Regul Integr Comp Physiol. Abbasnezhad, A, Hasanavand, A, Falahi, E, Kashkooli, S, Asbaghi, O, and Choghakhori, R.
Effect of L-Carnitine Supplementation on Lipid Profiles of Patients with Liver Disease: A Systematic Review and Meta-Analysis. Prev Nutr Food Sci. Yousefinejad, A, Siassi, F, Mirshafiey, A, Eshraghian, MR, Koohdani, F, Javanbakht, MH, et al.
Effect of Genistein and L-Carnitine and Their Combination on Gene Expression of Hepatocyte HMG-COA Reductase and LDL Receptor in Experimental Nephrotic Syndrome. Iran J Public Health. PubMed Abstract Google Scholar.
BMC L-carjitine volume 20Anf number: Natural thermogenesis triggers this Natural thermogenesis triggers. Metrics Noninvasive glucose monitor. l -carnitine is emerging as an item of interest for cardiovascular disease CVD prevention and treatment, but controversy exists. To examine the effectiveness and safety of l -carnitine, we assessed how genetically different levels of l -carnitine are associated with CVD risk and its risk factors. Given higher CVD incidence and l -carnitine in men, we also examined sex-specific associations. We used Mendelian randomization to obtain unconfounded estimates.
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