Fig. 3

Paternal iAs alters hepatic lipid metabolic gene expression and sex hormones in F1 offspring. (a-c) RT-qPCR analysis of genes in fatty acid oxidation (FAO), lipogenesis, and lipolysis in the liver of F1 females (F1-F) after 7 h fasting or 7 h refed conditions, n = 3 mice for control groups and n = 4 for iAs groups. The mean value in the con-Refeed groups was set as 1. (d-f) RT-qPCR analysis of genes in FAO, lipogenesis, and lipolysis in the liver of F1 males (F1-M), n = 4 mice control groups and n = 5 for iAs groups. (g)¹⁴ C-acetate tracer analysis of de novo lipogenesis (DNL) in primary hepatocytes from F1 females at 22 weeks old, n = 4 mice. (h)³ H-palmitate tracer analysis of FAO in primary hepatocytes from F1 females at 22 weeks old, n = 3–4 mice. (i)¹⁴ C-acetate tracer analysis of DNL in primary hepatocytes from F1 males at 22 weeks old, n = 4 mice. (j)³ H-palmitate tracer analysis of FAO in primary hepatocytes from F1 males at 22 weeks old, n = 4 mice. (k-l) Serum follicle-stimulating hormone (FSH) and estradiol levels in F1 females, n = 10 mice. Two-way ANOVA with the Holm-Sidak method was used to analyze gene expression levels. Two-sided t-test was used to analyze isotope tracer assays, serum FSH levels, and serum estradiol levels. Data are mean ± S.E.M. * P < 0.05 between conF1 and iAsF1 groups under the same conditions