The normal activities of maternal thyroid hormones (THs) are needed for the fetal/ neonatal development (El-bakry et al., 2010; Ahmed, 2011, 2012a,b, 2013, 2014, 2015a-c, 2016a-d, 2017a-v & 2018a-i; Ahmed et al., 2008, 2010, 2012, 2013a,b, 2014; 2015a,b& 2018a,b; Ahmed and Ahmed, 2012; Ahmed and Incerpi, 2013;Van Hercket al., 2013; Ahmed and El-Gareib, 2014,Incerpi et al., 2014; Candelotti et al., 2015; De Vito et al., 2015; El-Ghareeb et al., 2016; Ahmed and El-Gareib, 2017; Gigena et al., 2017), particularly the hepatic function, lipid homeostasis, the basal metabolic rate of hepatocyte, and the bilirubin metabolism (Huang and Liaw, 1995; Malik and Hodgson, 2002; Tindall et al., 2007; Paquette et al., 2011; Yao et al., 2014).In addition, the liver has a significant action in THs metabolism by deiodinases (D1, D2 and D3) (Malik and Hodgson, 2002; Tindall et al., 2007; Paquette et al., 2011; Ahmed, 2012b; Bano et al., 2016). The alterations in hepatic lipid homeostasis due to the abnormality in thyroid states might cause a non-alcoholic fatty liver disease (NAFLD; a very common liver disorder) (Liu et al., 2007; Burra, 2013). These changes were a dosedependent manner (Chung et al., 2012). Though, the direct relationship between the pathogenesis of NAFLD and thyroid disorders is still unknown. On the other hand, thyroid disorders may disturb the liver function (Malik and Hodgson, 2002), glycogen accumulation and hepatic fatty acid composition (Yao et al., 2014), and elevate the alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase (Huang and Liaw, 1995).