Abstract
Specific miRNA expression profiles have been shown to be associated with nonalcoholic fatty liver disease (NAFLD). We examined the correlation between the circulating levels and hepatic expression of miR122 and miR33a/b*, the key lipid metabolism-related gene expression and the clinicopathological factors of obese women with NAFLD. We measured miR122 and miR33a/b* expression in liver samples from 62 morbidly obese (MO), 30 moderately obese (ModO), and eight normal-weight controls. MiR122 and miR33a/b* expression was analyzed by qRT-PCR. Additionally, miR122 and miR33b* circulating levels were analyzed in 122 women. Hepatic miR33b* expression was increased in MO compared to ModO and controls, whereas miR122 expression was decreased in the MO group compared to ModO. In obese cohorts, miR33b* expression was increased in nonalcoholic steatohepatitis (NASH). Regarding circulating levels, MO patients with NASH showed higher miR122 levels than MO with simple steatosis (SS). These circulating levels are good predictors of histological features associated with disease severity. MO is associated with altered hepatic miRNA expression. In obese women, higher miR33b* liver expression is associated with NASH. Moreover, multiple correlations between miRNAs and the expression of genes related to lipid metabolism were found, that would suggest a miRNA-host gene circuit. Finally, miR122 circulating levels could be included in a panel of different biomarkers to improve accuracy in the non-invasive diagnosis of NASH.
Highlights
Nonalcoholic fatty liver disease (NAFLD), the hepatic consequence or precursor of type 2 diabetes and metabolic syndrome, is the most common chronic liver disease in developed countries [1,2,3]
The cohort was first classified according to the degree of obesity: normal-weight (body mass index (BMI) < 25 kg/m2), moderately obese (ModO) (BMI 32–38 kg/m2), and morbidly obese (MO) subjects (BMI > 40 kg/m2)
Biochemical analyses indicate that ModO and MO women had significantly higher levels of homeostatic model assessment 2-insulin resistance (HOMA2-IR), glucose, insulin, HbA1c, and triglycerides than the control group
Summary
Nonalcoholic fatty liver disease (NAFLD), the hepatic consequence or precursor of type 2 diabetes and metabolic syndrome, is the most common chronic liver disease in developed countries [1,2,3]. The incidence of NAFLD has increased alarmingly over the last twenty years worldwide In developed countries, it is between 10% and 30%, and can be as high as between 60% and over 90% among obese subjects [4,5]. Adipose tissue and gut, producing and releasing circulating endotoxins, adipokines, and pro-inflammatory cytokines, which contribute to insulin resistance (IR) and free fatty acids accumulation, may induce oxidative stress and hepatocellular damage [9,10,11] Among all these “multiple parallel” mechanisms, a deregulation of the lipid metabolism seems to play a crucial role in the pathogenesis of NASH [12]
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