Defined Diets Link Iron and α-Linolenic Acid to Cyp1b1 Regulation of Neonatal Liver Development Through Srebp Forms and LncRNA H19.

substantially affects hepatic vascular and stellate cells (HSC) with linkage to liver fibrosis. Despite minimal hepatocyte expression, deletion substantially impacts liver gene expression at birth and weaning. The appreciable expression in surrounding embryo mesenchyme, during early organogenesis, provides a likely source for . Here defined breeder diets established major interconnected effects on neonatal liver of α-linolenic acid (ALA), vitamin A deficiency (VAD) and suboptimal iron fed mice. At birth and VAD each activated perinatal HSC, while suppressing iron control by hepcidin. deletion also advanced the expression of diverse genes linked to iron regulation. Postnatal stimulations of -regulated genes in the fatty acid and cholesterol biosynthesis pathways were suppressed by -deficiency. and the neutrophil alarmin expression increased due to slower postnatal decline with deficiency. VAD reversed each of effect, probably due to enhanced HSC release of Apo-Rbp4. At birth, deletion enhanced participation. Notably, a suppressor () decreased while an activity partner (/H3K methylation) increased expression. ALA elevated hepcidin mRNA and countered the inhibitory effects of deletion on hepcidin expression. Oxylipin metabolites of ALA from highly expressed hepatic are potential mediators. expression patterns demonstrated female dimorphism for neonatal liver. Mothers followed one of three fetal growth support programs probably linked to maturity at conception.