Serum and urine DCA concentrations were statistically significantly increased. Patients with NASH exhibited a greater postprandial increase in all bile acid groups except LCA and 6α-hydroxylated bile acids. Patients with NASH had decreased glycine- and taurine-conjugated LCA exposure over the postprandial period.
Etiocholanolone-S, DHEA-2S, and DHEA-S decreased with the progression of fibrosis, while 16-OH-DHEA-S increased with the progression of fibrosis. The ratio of 16-OH-DHEA-S to DHEA-S (16/D) and the ratio of 16-OH-DHEA-S to etiocholanolone-S (16/E) were more clearly associated with the fibrosis grade.
Strong overlap of the animal model samples and human NAFLD patients is observed in the sn-1 monoacylglycerophosphocholine profile. Seven sphingomyelin type lipids: (SM 36:3), (d18:2/16:0), (d18:2/14:0), (d18:1/18:0), (d18:1/16:0), (d18:1/12:0), and (d18:0/16:0) were found to be significantly altered in the human NAFLD patients compared to normal liver subjects; similar tendencies were also found in the animal model samples. Deoxycholic acid was found significantly higher both in the animal model samples and in the human NAFLD patients.
Hydroquinone (HQ) and nicotinic acid (NA) suggest a protective effect against NAFLD. However, only NA showed marked effects on both steatosis and transaminase levels suggesting its potential as a therapeutic or preventive agent in NALFD.
Stearoylcarnitine increased notably in both rat liver tissue and serum. However, the potential as biomarker of NAFLD still needs to be confirmed by extensive studies.
Four potential biomarkers for diagnosis of NAFLD stages were selected: serum glucose, lactate, glutamate/glutamine, and taurine. A specific combination of spectroscopic changes in glucose, lactate, glutamate/glutamine, and taurine levels may prove to be an accurate means of noninvasively diagnosing various stages of NAFLD.
