Effect of Coenzyme Q10 on the Outcome of Metabolic Dysfunction-Associated Fatty Liver Disease Patients

The liver disease with the most continuously rising prevalence rates is metabolic-dysfunction associated fatty liver disease (MAFLD), making us arrive at a conclusion that it might be the liver disease epidemic of the 21st century. It is increasingly diagnosed in many developed and developing countries and is considered the most common cause of chronic liver disease among patients with type 2 diabetes mellitus (T2DM). By 2030, it will be the leading cause for hepatocellular carcinoma (HCC) related liver transplantation (LTx) in western countries.

A number of studies have suggested that metabolic associated co-morbidities, such as obesity, type 2 DM, CVD, dyslipidemia, hypertension, metabolic syndrome, hypothyroidism, OSAS, PCOS are major risk factors for MAFLD.

It encompasses a wide spectrum of histological pattern, ranging from simple steatosis to steatohepatitis, fibrosis and cirrhosis.

The global prevalence of MAFLD is currently estimated to be 25%, but the highest rates are reported from the Middle East 31.8% and South America 30.5%, followed by Asia 27.4%, the USA 24% and Europe 23.7%, whereas MAFLD is less common in Africa 13.5%.

Coenzyme Q10 (CoQ10) or ubiquinone is a lipid-soluble and vitamin-like compound, which acts as a pivotal cofactor in the mitochondrial respiratory chain in addition to its role as a natural scavenger of free radicals. It is synthesized by cells of the body and also found in abundance in the human diet. Recent evidence suggests that CoQ10 supplementation might be useful in improving and preventing pathological conditions such as metabolic syndrome, hypertension, diabetes, liver diseases, and insulin resistance Because of its antioxidant activity, it seems that CoQ10 can prevent activation of the inflammatory signaling pathway. Many studies have shown that administration of CoQ10 reduced hepatic oxidative stress and inflammation. Also, other studies observed that CoQ10 supplementation reduced TNF-α production and serum levels of liver aminotransferase and decreased NF-kB expression. In addition, a previously published study showed that a dose of 100 mg/day of CoQ10 for 4 weeks can improve serum AST levels, total antioxidant capacity and waist circumference, but it had a non-significant effect on insulin resistance and MDA levels. The same result was found in the study by Esfahani et al. reporting improvement in AST and ALT concentrations and lower grades of portal inflammation and hepatocellular liver necrosis in thioacetamide-induced liver damage in rats. Yet, some contradicting results were reported by Hodgson et al. were they found a non-significant reduction in body weight after CoQ10 supplementation in patients with T2DM. These contradictions were addressed by Faresi et al. where they tested the effect of the same oral dose of CoQ10 used by Farhangi et al. for 12 weeks, where it had beneficial effects on serum levels of TNF-a, hs-CRP, hepatic enzymes, adiponectin, and NAFLD grades as well as near-significant changes in serum leptin among patients with NAFLD. However, serum IL-6 levels and AAR remained unchanged after CoQ10 supplementation.