Livers from NASH-fed rats weighed significantly more compared to Control (p < 0.0001), HFD (p < 0.0001) and HFr (p < 0.001, Table 3), as did livers from HFr-fed rats compared to HFD (p < 0.05). Hepatic TG content was higher in NASH- and HFD-fed rats compared to both Control (p < 0.01 and p < 0.0001) and HFr (p < 0.01 and p < 0.0001, Fig. 2b). Additionally, HFD-fed animals had higher hepatic TG levels compared to NASH (p < 0.01). Hepatic TG levels in rats fed HFr did not differ from those fed the Control diet. Hepatic TC levels were significantly elevated in NASH-fed animals compared to Control, HFD, and HFr (p < 0.0001, Fig. 2c). Liver glycogen was significantly lower in both NASH and HFD compared to Control and HFr (p < 0.0001, Fig. 2d). At week 16, ALAT-levels were significantly higher in NASH-fed rats compared to Control- (p < 0.0001, Fig. 3a), HFD- and HFr-fed rats (p < 0.01). Plasma levels of ASAT were higher in the NASH-group compared to both Control- and HFr-groups (p < 0.05, Fig. 3b). Furthermore, plasma levels of the β-oxidation marker β-hydroxybuturate were increased in HFD-fed rats compared to Control-, NASH- and HFr-groups (p < 0.0001, p < 0.01 and p < 0.0001, Table 3).Table 3Metabolic and inflammatory effects in rats after 16 weeks on NASH-, HFD- and HFr-dietControlNASHHFDHFrLiver weight (g)18.9 ± 3.4#32.7 ± 7.9*†‡16.5 ± 2.5# ‡23.1 ± 4.4#†Fasting plasma glucose (mM)b6.4 ± 0.2#†‡7.2 ± 0.2*7.5 ± 0.1*7.16 ± 0.2*Fasting plasma insulin (pM)b560.6 ± 79.5486.7 ± 93.7603.0 ± 43.7695.8 ± 83.7Plasma β-hydroxybutyrate (µmol/L)38.4 ± 4.2†64.0 ± 5.3†115.4 ± 16.8*#‡38.4 ± 2.8†Plasma leptin (ng/mL)3283.3 ± 1035.2†3803.0 ± 1341.1†9366.6 ± 2052.8*#‡2638.0 ± 808.5†Plasma TG (mmol/L)1.6 ± 0.2‡1.7 ± 0.1‡1.5 ± 0.1‡3.9 ± 0.5*#†Plasma FFA (mmol/L)0.3 ± 0.10.4 ± 0.030.4 ± 0.020.3 ± 0.02Plasma Cholesterol (mmol/L)2.1 ± 0.12.5 ± 0.12.1 ± 0.12.3 ± 0.2Plasma HDL-C (mmol/L)1.3 ± 0.11.0 ± 0.11.3 ± 0.11.1 ± 0.1Jejunal MCP-1 (ng/mL)a45.3 [36.3; 55.3]58.1 [48.5; 69.6]49.5 [40.1; 60.5]56.4 [48.1; 65.5]Jejunal TNF-α (ng/mL)a179.9 [129.3; 247.7]87.6 [61.7; 125.5]171.1 [76.1; 384.6]213.2 [112.4; 404.3]Adipose tissue MCP-1 (ng/mL)a14.8 [13.4; 16.5]14.1 [11.9; 16.8]‡14.2 [11.3; 17.7]‡25.6 [15.2; 42.6]#†Adipose tissue TNF-α (ng/mL)a15.4 [14.4; 16.4]16.1 [14.3; 18.2]15.4 [13.6; 18.2]16.2 [14.6; 18.0]TG triglycerides, FFA free fatty acids, HDL-C high-density-lipoprotein-cholesterol, MCP-1 monocyte-chemoattractant-protein-1, TNF-α tissue-necrosis-factor-alphaResults are presented as mean ± SEM. Metabolic parameters denoted with superscript a, were analysed on log-transformed data (due to non-normal distribution), and are consequently presented as geometric means with 95% confidence intervals. Superscripts (*,#,†,‡) indicate significant (p < 0.05) differences in readouts compared to Control-, NASH-, HFD- and HFr-groups respectively. Sample sizes at week 16: n = 6–10/group. b Fasting plasma glucose and fasting plasma insulin levels were assessed after 15 weeks Fig. 3Markers of hepatic function, inflammation and fibrosis. a After 16 weeks ALAT-levels were significantly higher in NASH-fed rats compared to Control-, HFD- and HFr-fed rats. b Plasma levels of ASAT were higher in the NASH-group compared to both Control and HFr-groups. c Rats on NASH, HFD and HFr-diet had increased hepatic levels of MCP-1 compared to Control. d Hepatic TNF-α levels were significantly increased in the HFD fed rats compared to Control. e Haptoglobin was significantly increased in plasma of NASH-fed rats compared to rats fed Control, HFD and HFr. f Plasma TIMP-1 was significantly increased in the NASH-fed rats, compared to all other groups. Statistical significance: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Results are shown as mean ± SEM