Aghajani Taha, Arefhosseini Sara, Ebrahimi-Mameghani Mehrangiz, Safaralizadeh Reza
Department of Animal Biology, Faculty of Natural Sciences University of Tabriz Tabriz Iran.
Student Research Committee Tabriz University of Medical Sciences Tabriz Iran.
Food Sci Nutr. 2024 Jul 16;12(10):7177-7185. doi: 10.1002/fsn3.4267. eCollection 2024 Oct.
Insulin resistance (IR) is the pivotal pathological hit in non-alcoholic fatty liver disease (NAFLD). There is specific attention to combination/conjugated therapies for NAFLD management. As myo-inositol (MI) has been shown to improve IR in animal and human trials, this study aimed to investigate the influence of MI supplementation on glycemic response and IR through AMPK/PI3K/AKT signaling pathway in obese patients with NAFLD. This double-blinded placebo-controlled randomized clinical trial was conducted on 48 obese (BMI = 30-40 kg/m) patients with NAFLD who were randomly assigned to receiving either MI (4 g/day) or placebo (maltodextrin 4 g/day) group for 8 weeks. Before and after the trial, weight, height, serum glycemic parameters (inc. fasting glucose and insulin) as well as IR indices were assessed. Moreover, the mRNA expression levels of AMPK, AKT, and PDK-1 in peripheral blood mononuclear cells (PBMCs) were determined. MI supplementation resulted in significant increases in the fold changes of AMPK, AKT, and PDK-1 genes ( = .019, = .049, and = .029, respectively). Indeed, IR improved in terms of all IR indices in MI group ( < .05) after adjusting for the confounders, apart from quantitative insulin sensitivity check index (QUICKI). The results showed that MI supplementation not only upregulated AMPK, AKT, and PDK-1 mRNA in PBMCs but also improved IR in obese patients with NAFLD.
胰岛素抵抗（IR）是非酒精性脂肪性肝病（NAFLD）的关键病理因素。NAFLD的联合/共轭治疗受到了特别关注。由于在动物和人体试验中已证明肌醇（MI）可改善IR，本研究旨在通过AMPK/PI3K/AKT信号通路，探讨补充MI对NAFLD肥胖患者血糖反应和IR的影响。这项双盲安慰剂对照随机临床试验对48例NAFLD肥胖患者（BMI = 30 - 40 kg/m）进行，这些患者被随机分为接受MI（4 g/天）或安慰剂（麦芽糖糊精4 g/天）组，为期8周。在试验前后，评估体重、身高、血清血糖参数（包括空腹血糖和胰岛素）以及IR指标。此外，还测定了外周血单核细胞（PBMCs）中AMPK、AKT和PDK - 1的mRNA表达水平。补充MI导致AMPK、AKT和PDK - 1基因的倍数变化显著增加（分别为 = 0.019、 = 0.049和 = 0.029）。事实上，在调整混杂因素后，MI组除定量胰岛素敏感性检查指数（QUICKI）外，所有IR指标方面的IR均有所改善（ < 0.05）。结果表明，补充MI不仅上调了PBMCs中AMPK、AKT和PDK - 1的mRNA，还改善了NAFLD肥胖患者的IR。
