Histological staining's, and commercially available kits for serum ALT and AST and hepatic contents of TG, TC, MDA, SOD, and GSH were used to assess NASH.
Supplementation of 1,25(OH)<sub>2</sub>D<sub>3</sub> in CDHF-diet mice showed decreased serum levels of ALT, AST, indicating the improvement in overall liver function, and suppressed histological NASH regarding fibrosis stage, lobular inflammation, and steatosis compared to the OVX group.
In addition, HIF1α silencing significantly decreased HIF1α, biochemical indices (ALT, AST, and TG), inflammatory factors (TNFα, IL6, and IL1β), and angiogenesis indices (CD34 and VEGFR2), consequently, improved the hepatic fibrosis score in the rat model of combined hypoxia and NASH.
The classification performance of validated miRNAs (and their ratios) for NASH was better than that reached by AST, whereas for advanced fibrosis prediction miRNAs did not perform better than the FIB-4 algorithm.
Those with NASH had significantly higher (p < 0.05) pre-VLCD ALT, AST, insulin resistance, and proportion of individuals with diabetes compared to those with NL.
Meanwhile, BP increased the levels of SOD (superoxide dismutase), GSH (reduced glutathione) and HDL-C (high-density lipoprotein cholesterol), and reduced the levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), TG (triglycerides), LDL-C (low-density lipoprotein cholesterol) and MDA (malondialdehyde) in NASH models (<i>p</i> < 0.05).
In multivariate analysis, triglyceride and HDL cholesterol were predictors of NASH in patients with genotype 1, whereas in patients with genotype 3, AST was the only predictor.