Fig. 2
Acoustic impedance analysis. a Mouse. (a-1) Liver sample: the acoustic impedance (× 106 kg/m2/s) showed a gradual decrease from control (median 1.715, IQR 0.06), SS (median 1.68, IQR 0.05), to NASH (median 1.635, IQR 0.025), showing differences between control and SS (p = 0.554), control and NASH (p = 0.039), and SS and NASH (p = 0.113). (a-2) FFA in the liver: the ratio of sum of percentage composition of FFAs between the low-impedance group and the high-impedance group showed gradual increases from control (median 4.45, IQR 0.65; 3.58–4.87), SS (median 7.92, IQR 0.322; 7.23–8.39), to NASH (median 9.9, IQR 0.73; 8.94–11.2), with significant differences between control and SS (p = 0.0002), control and NASH (p < 0.001), and SS and NASH (p = 0.003). White, low-impedance group; gray, high-impedance group. Data are presented as mean and standard deviation. b Human liver sample. (b-1) Liver sample: the acoustic impedance (× 106 kg/m2/s) showed gradual decrease from control (median 1.825, IQR 0.015), SS (median 1.788, IQR 0.0045), to NASH (median 1.76, IQR 0.015), showing differences between control and SS (p = 0.023), control and NASH (p = 0.003), and SS and NASH (p = 0.050). (b-2) Free fatty acids in the liver: the ratio of sum of percentage composition of FFAs between the low-impedance group and the high-impedance group showed a gradual increase from control (median 5.7, IQR 0.012; 5.53–5.73), SS (median 5.9, IQR 0.0029; 4.23–7.75), and NASH (median 6.2, IQR 0.0021; 5.3–6.8). However, there were no significant differences between control and SS (p = 0.758), control and NASH (p = 0.671), and SS and NASH (p = 0.893). White, low-impedance group; gray, high-impedance group. Data are presented as mean and standard deviation. FFA Free fatty acid, IQR Interquartile range, NASH Nonalcoholic steatohepatitis, SS Simple steatosis