The HFHC diet–fed and HF diet–fed mice consumed more total calori

The HFHC diet–fed and HF diet–fed mice consumed more total calories

per day (12.54 ± 0.6 and 11.76 ± 1.5 kcal/day, respectively) than their chow-fed controls (8.67 ± 1.6). There was no difference between HF and HFHC in terms of total calories consumed or stool output per day. Percent fat content in fecal material was also similar between the HF (2.46 ± 0.6%) and HFHC (2.08 ± 0.7%) groups. Mice fed HFHC and HF diets gained more weight than mice fed the chow diet. HFHC and HF mice had mean body weights of 50.5 ± 0.8 g and 53.18 ± 1.8 g, respectively (Fig. 1A), compared with a mean body weight of 31.94 ± 0.2 g for chow-fed mice at 16 weeks. Total body fat mass estimation by way of magnetic resonance imaging at 12 weeks demonstrated that HFHC mice (18.66 ± 0.7 g) and HF mice (18.40 ± 0.9 g) had significantly greater body fat compared with chow-fed see more mice (2.82 ± 0.6 g; P < 0.0001) (Fig. 1B). Fasting plasma glucose levels were higher in HFHC (223.6 ± 7 mg/dL) and HF (235.4 ± 10 mg/dL) mice than in chow-fed mice (160.4 ± 7.3 mg/dL; P < 0.0001) (Fig. 1C). Similarly, fasting insulin was higher in HFHC mice (7.7 ± 1 ng/mL) and

HF mice selleck screening library (10.3 ± 0.9 ng/mL) compared with chow-fed mice (1.9 ± 0.1 ng/mL; P < 0.0001) (Fig. 1D). Glucose and insulin values were used to estimate insulin resistance as HOMA-IR calculations, and both HFHC (4.2 ± 0.6) and HF (5.9 ± 0.5) mice were significantly insulin-resistant compared with chow-fed mice (1.1 ± 0.4; P < 0.0001) (Fig. 1E). Thus, both HFHC and HF mice were significantly obese and insulin-resistant compared with chow mice. Histologic examination of livers from HFHC and HF mice demonstrated substantial steatosis with inflammatory changes. Microvesicular and macrovesicular learn more steatosis were clearly visible on routine histology staining with hematoxylin-eosin after 16 weeks (Fig. 2A). For sections with a steatosis score of 3, the distribution of steatosis in both the HF group and the HFHC group was panlobular. Nearly all hepatocytes have microvesicular steatosis, and many had both microvesicular and macrovesicular steatosis with a random distribution. For sections with a steatosis score ≤2, there was

a panlobular distribution of steatosis in the HF group, but there was evidence of zone II sparing in the HFHC group. Lobular inflammation was prominent in HFHC sections similar to human NASH descriptions (Fig. 2B). Confirming the histological impressions, the weights of the livers of HFHC and HF mice were significantly higher compared with chow-fed mice (P < 0.0001) (Fig. 2E). Similarly, TG content at 16 weeks was higher in HFHC mice (1,955 ± 430 mg/dL per 100 mg wet liver) and HF mice (1,096 ± 115) compared with chow mice (276 ± 34; P < 0.0001 [one-way ANOVA]) (Fig. 2C). Plasma ALT levels were also greater in both HFHC (217.3 ± 40.2 IU/L) and HF mice (187 ± 47 IU/L) at 16 weeks compared with chow-fed mice (70.9 ± 5.4 IU/L; P < 0.0001) (Fig.

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