ABSTRACT: Non-alcoholic fatty liver, a chronic inflammatory disease, is accompanied by accommodation of extra fat and occurrence of oxidative stress in liver. L-carnitine with antiinflammatory and anti-oxidant properties may have beneficial effects on NASH. This study was designed to assess the antioxidant and anti-inflammatory effects of L-carnitine on NASH patients' conditions. This randomized double-blind placebo-controlled clinical trial was performed in 68 patients suffering from NASH and 34 control subjects. NASH patients were randomly divided into groups of L-carnitine (receiving 2000 mg L-carnitine supplements) (n=36), placebo (n=32). Fasting blood samples were taken at study baseline and after 12 weeks of intervention to quantify inflammatory factors and malondialdehyde. L-carnitine supplementation resulted in a significant reduction in serum malondialdehyde (MDA) (-9.93[+ or -]3.79 vs. +1.76[+ or -]2.93 and +0.16[+ or -]2.44 [micro]mol/L, P=0.01) compared with placebo and control groups. Within-group comparisons revealed a significant reduction in serum high sensitivity C-Reactive Protein (hs-CRP) (P=0.02), Transforming Growth Factor-[beta] (TGF-[[beta].sub.1] ) (P=0.02), Tumor Necrosis Factor-[alpha] (TNF-[alpha]) (P= 0.004) and Malondialdehyde (MDA) (P=0.01) levels in the L-carnitine group. After adjusting for covariates, significant decreases of hs-CRP, TNF-[alpha] and MDA were found in the L-carnitine group compared to placebo and control groups. In conclusion, L-carnitine supplementation for 12 weeks among patients suffering from NASH had beneficial effects on MDA, TNF-[alpha] and hs-CRP levels; however, it did not affect TGF-[B.sub.1].
KEYWORDS: L-Carnitine, Inflammatory factors, NASH
Non-alcoholic fatty liver disease (NAFLD) with accumulation of extra fat in liver (Kelishadi et al., 2013) is the most common liver disease in the world (Fruci et al., 2013). NASH prevalence is 10-24% among the general population and 75% in obese people (Clark and Diehl, 2003, LUDWIG et al., 1997). NASH is considered to be the hepatic manifestation of metabolic syndrome (Falck-Ytter et al., 2001). Compared to limited clinical, laboratory and radiological tests, liver biopsy is the golden standard for definite NAFLD and NASH diagnosis (Younossi, 2008). Multiple factors are involved in pathogenesis of NASH. The depositions of fatty acid in liver and decreased hepatic fatty acid oxidation or increased hepatic lipogenesis are the initial symptoms of NASH (Edmison and McCullough, 2007). Also, there is oxidative stress resulting from mitochondrial reactive oxygen species and endogen toxins (Edmison and McCullough, 2007). Pro-inflammatory cytokines have an important role in the development and progression of fatty liver disease (Epstein et al., 2000). Oxidative stress and reactive oxygen species increase lipid peroxidation in hepatocyte membrane and leads to the release of pro-inflammatory cytokines and fibrosis (Younossi, 2008, Videla et al., 2004). Several mechanisms such as apoptotic pathways have been suggested in the pathogenesis of NASH. (Wieckowska et al., 2006). Adipo-cytokines seem to be involved in NASH development and several studies have revealed high levels of pro-inflammatory cytokines (Jarrar et al., 2008). For example, treatments triggered by tumor necrosis factor-[alpha] (TNF-[alpha]) showed beneficial effects on the improvement of NASH (Epstein et al., 2000, Satapathy et al., 2004).
Various strategies for controlling NAFLD have been suggested including nutritional counseling, gradual weight loss, physical activity (Yoneda et al., 2006), insulin...
This is a preview. Get the full text through your school or public library.