Fig. 7
Liver ERα/β in F1 females counteracts the lipid metabolic changes of paternal iAs. (a) Liver triglyceride (TG) contents in F1 females injected with AAV-GFP, n = 4–5 mice. (b) Serum TG levels in F1 females injected with AAV-GFP, n = 8 mice. (c) Serum non-esterified fatty acids (NEFAs) levels in F1 females injected with AAV-GFP, n = 11 mice. (d) Liver TG contents in F1 females injected with AAV-Cre, n = 4 mice. (e) Serum TG levels in F1 females injected with AAV-Cre, n = 8 mice. (f) Serum NEFAs levels in F1 females injected with AAV-Cre, n = 9–11 mice. (g-l) RT-qPCR analysis of genes in fatty acid oxidation (FAO), lipogenesis, and lipolysis in fasting or refed condition in the liver of F1 females injected with AAV-GFP or AAV-Cre, n = 4–5 mice. The mean values in the con-GFP or con-Cre group were set as 1. (m-n)3 H-palmitate tracer analysis of FAO in primary hepatocytes from F1 female mice at 30 weeks old injected with AAV-GFP or AAV-Cre, n = 3–4 mice. (o-p)14 C-acetate tracer analysis of de novo lipogenesis (DNL) in primary hepatocytes from F1 female mice at 30 weeks old injected with AAV-GFP or AAV-Cre, n = 3 mice. Two-way ANOVA with the Holm-Sidak method was used to analyze liver TG, serum TG, serum NEFAs, and gene expression levels. Two-sided t-test was used to analyze isotope tracer assays. Data are mean ± S.E.M. * P < 0.05 between conF1 and iAsF1 groups under the same conditions