The effect of Myo-inositol supplementation on plasma visfatin, insulin sensitivity and atherogenic indices in patients with non-alcoholic fatty liver disease

Abstract

Abstract Introduction: Non-alcoholic fatty liver disease (NAFLD) - the most common chronic liver disease with a prevalence of 32% in the general population- is the main cause of death in most countries. This disease includes a wide range of liver complications, including hepatic steatosis to cirrhosis and hepatocellular carcinoma, and causes irreparable damage. Obesity, insulin resistance, and pro-inflammatory adipokines play a role in the pathogenesis of this disease. Recently, supplementation of the inositol family, especially Myo-inositol (MI), has shown antioxidant, anti-diabetic, and anti-inflammatory properties. Therefore, this study aimed to investigate the effects of MI supplementation on visfatin plasma level, insulin sensitivity and atherogenic indicators in patients with NAFLD . Methods: In this double-blind randomized clinical trial, 42 eligible obese patients with NAFLD were randomly allocated into MI and placebo groups (n=21 in each group) and received two 2g MI or maltodextrin as placebo sachets per day for 8 weeks associated with dietary recommendations. Personal details for each patient were collected at baseline. Before and after the intervention,a physical activity questionnaire (IPAQ-SF) and a 3-day food recall were completed and anthropometric measurements and body composition were assessed. Blood sampling after 12-14 hours fasting was taken to determine glycemic indices (glucose (FBS), insulin), lipid profile (triglyceride (TG), total cholesterol (TC), high- and low-density lipoprotein (HDL-C, LDL-C)), visfatin and aspartate- and alanine- aminotransferases (AST and ALT) were assessed. Then, atherogenic indices and insulin sensitivity index (Quicki) were estimated. Results: At the end of the study, the significant decrease in the amount of fat-free mass (P=0.044) in the MI group, after adjustment for baseline values and the difference in energy intake, was significantly higher than the placebo group. While, no significant difference was found in energy and macronutrient intake, weight, Body mass index (BMI), and body fat mass. Although, at the end of the study no significant difference was found in visfatin plasma level between the group receiving MI and placebo; but changes in visfatin plasma level and changes in fat intake (P=0.021, r=-0.50), cholesterol intake (P=0.005, r=-0.50) and insulin (P=0.025, r=-0.49) were statistically significant (P<0.05). At the end of the study, supplementation with MI compared to placebo caused a significant decrease in serum glucose concentration (P=0.001), after adjustment for baseline values and the difference in energy intake, but it did not have a significant effect on the Quicki index. However, the changes in atherogenic indices and liver enzymes in the group receiving MI and placebo were not significant; a marginally significant decrease in AST serum levels was found after adjustment for confounding factors (P=0.057). Conclusion: Although supplementation with MI led to a decrease in fat-free mass and fasting glucose levels in patients with NAFLD, it did no effect on insulin sensitivity, atherogenic indices, and plasma visfatin. Keywords: Non-alcoholic fatty liver disease, Myo- inositol, visfatin, insulin sensitivity, atherogenic indices.