Effect of L-Carnitine Supplementation on Liver Enzymes: A Systematic Review and Meta-analysis of Randomized Controlled Trials.
Possible Hepato-protective effects of L-carnitine have been reported in previous studies. Present study was conducted to systematically review the efficacy of L-carnitine supplementation on liver enzymes.
The following databases were searched up to December 2018: PubMed, Scopus, ISI Web of Science, and the Cochrane library. Only randomized controlled trials (RCTs) evaluating the effects of L-carnitine supplementation on liver enzymes including alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) were included. Pooled effect size measured using random effect model (Dersimonian-Liard).
A total of 16 studies (including 1025 participants) were included in the present meta-analysis. Pooled analysis indicated that L-carnitine supplementation significantly decreased ALT (weighted mean difference (WMD): -10.729 IU/L, 95% CI: -13.787, -7.672, p <0.001; I2 = 95.9%), AST (WMD: -7.149 IU/L, 95% CI: -9.202, -5.096, p <0.001; I2 = 93.5%) and GGT (WMD: -7.395: IU/L, 95% CI: -9.171, -5.619, p <0.001; I2 = 80.1%). Subgroup analysis revealed that effect of L-carnitine supplementation on liver enzymes was not significant in normal weight and healthy subjects. Baseline BMI and health status were the potential source of heterogeneity.
L-carnitine supplementation showed beneficial hepato-protective effects on circulating liver enzymes.
Askarpour M
，Djafarian K
，Ghaedi E
，Sadeghi O
，Sheikhi A
，Shab-Bidar S
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The effects of carnitine supplementation on clinical characteristics of patients with non-alcoholic fatty liver disease: A systematic review and meta-analysis of randomized controlled trials.
The beneficial effects of carnitine supplementation on nonalcoholic fatty liver disease are unclear. We conducted a systematic review and meta-analysis to evaluate the effects of carnitine supplementation on liver function, lipid profile, body mass index, body weight, and homeostasis model assessment of insulin resistance in patients with nonalcoholic fatty liver disease.
A comprehensive search of PubMed, Web of Science, Scopus, Cochrane Library, and Google Scholar databases were performed. Only randomized placebo-controlled human studies that examined the effects of carnitine supplementation on liver function, lipid profile, body mass index, body weight, and homeostasis model assessment of insulin resistance up to September 2019 were included. Fixed effects or random-effects models were applied to compute the pooled effect size. Heterogeneity assessments were performed using Cochran's Q test and I-squared statistics. The quality of the studies was assessed using the Jaded scale.
A total of 5 articles were selected, including 334 individuals (167 in control and 167 in intervention groups). The results demonstrated that carnitine supplementation significantly reduced homeostasis model assessment of insulin resistance (HOMA-IR) (WMD: -0.91; 95 % CI: -1.11, -0.72; p < 0.001, I2 = 0.0 %) and the levels of aspartate aminotransferase (AST) (WMD: -16.62; 95 % CI: -28.11, -5.14; IU/l; p = 0.005, I2 = 93.5 %), alanine aminotransferase (ALT) (WMD: -33.39; 95 % CI: -45.13, -21.66; IU/l; p < 0.001, I2 = 93.4 %), and triglycerides (TG) (WMD: -22.13; 95 % CI: -38.91, -5.34; mg/dl; p = 0.01; I2 = 0.0 %). However, the results of the pooled effect size did not show any significant effect of carnitine supplementation on body mass index (BMI) (WMD: 0.07; 95 % CI: -0.15, 0.29; p = 0.55; I2 = 0.0 %), body weight (WMD: -0.28; 95 % CI: -2.23, 1.68; p = 0.78; I2 = 45.7 %), the levels of gamma-glutamyl transferase (γGT) (WMD: -11.31; 95 % CI: -24.35, 1.73; IU/l; p = 0.09, I2 = 61.1 %), cholesterol (WMD: -13.58; 95 % CI: -46.77, 19.60; mg/dl; p = 0.42; I2 = 94.9 %), high-density lipoprotein-cholesterol (HDL-C) (WMD: 1.36; 95 % CI: -0.96, 3.68; mg/dl; p = 0.25; I2 = 64.7 %), and low density lipoprotein-cholesterol (LDL-C) (WMD: -14.85; 95 % CI: -45.43, 15.73; mg/dl; p = 0.34; I2 = 96.4 %).
This analysis shows that carnitine supplementation for patients with nonalcoholic fatty liver disease demonstrates a reduction in AST, ALT, TG levels and HOMA-IR. However, no significant effect of carnitine supplementation was observed on BMI, body weight, the levels of γGT, TC, HDL-cholesterol and LDL-cholesterol.
Abolfathi M
，Mohd-Yusof BN
，Hanipah ZN
，Mohd Redzwan S
，Yusof LM
，Khosroshahi MZ
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The effect of melatonin supplementation on liver indices in patients with non-alcoholic fatty liver disease: A systematic review and meta-analysis of randomized clinical trials.
Several randomized clinical trials (RCTs) evaluated the effect of melatonin supplementation on liver enzymes in patients with non-alcoholic fatty liver disease (NAFLD) and reported conflicting results. To meet these discrepancies, a meta-analysis was conducted to evaluate the eff ;ect of melatonin on liver indices in patients with NAFLD. To collect the required data, a thorough search was conducted through Web of science, Pubmed, Cochrane database, Embase, Google Scholar, ProQuest, and Scopus databases. The aim was to find clinical trials over the effect of melatonin supplementation on liver indices up to 16 May 2019. As a result, five eligible articles were selected and analysed in this meta-analysis using a fixed-effects model. Heterogeneity test was performed by I2 statistics and Cochrane Q test. The results showed that melatonin had a significant effect on aspartate aminoteransferase (AST) (WMD = 2.29, [95 %CI: 1.14, 3.43] IU/L, p = <0.001), alkaline phosphatase (ALP) (WMD = -8.40, [95 %CI -11.33, -5.48] IU/L, p < 0.001), and gamma-glutamyltransferase (GGT) (WMD = -33.37, [95 %CI: -37.24, -29.49] IU/L, p= < 0.001). Melatonin had no significant effect on alanine aminotransferase (ALT) regarding the overall effect size. Based on this meta-analysis, melatonin supplementation can improve liver indices. However, more RCTs are required with larger sample sizes and better control of confounding variables such as weight, body mass index, and gender to determine the effect of melatonin on patients with non-alcoholic fatty acid disease.
Mansoori A
，Salimi Z
，Hosseini SA
，Hormoznejad R
，Jafarirad S
，Bahrami M
，Asadi M
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