PGC-1a and Ppara are transcription factors known to regulate these pathways in adults ; however, Yubero et al. found that changes in PGC-1a expression did not parallel hepatic lipid oxidation gene induction following initiation of suckling. Of the transcription factors we evaluated, only Ppara and Sirt3 were markedly induced at the onset of suckling. In rat liver, Ppara mRNA and protein increase after birth and remains enhanced during suckling. Our results show a similar pattern of Ppara mRNA expression in mouse liver with highest levels observed during the suckling ages. Thus, Ppara is a good candidate factor for the regulation of ketogenic and lipid oxidation pathways that are induced at the onset of suckling. Sirt3 may also play a role in this induction as this factor is known to activate enzymes of fatty acid oxidation and ketogenesis, and is implicated in the metabolic syndrome. Research into whether Sirt3 regulate ketogenesis, or lipid oxidation at birth is warranted. We are the first to describe an in-depth analysis of the ontogeny of lipid droplet and VLDL BLU-285 metabolism genes. Collectively, these pathways were upregulated after birth �C likely to accommodate the large R1487 Hydrochloride influx of lipids from milk. Lipid droplets are coated with proteins, such as perilipins, that are thought to regulate lipid droplet turnover by regulating lipolysis. Furthermore, lipid droplets and their associated proteins play a role in the development of insulin resistance, obesity, and the metabolic syndrome. In this study, we observed a brief, but stark increase in Plin2 expression coincident with the onset of suckling. Interestingly, Plin2-null mice are protected from dietinduced obesity and fatty liver disease, indicating a critical role for Plin2 in the development of metabolic diseases. Thus, identification of pathways that control expression of Plin2 may provide new therapeutic targets for the treatment of obesity and related disorders. Our study presents an interesting model to investigate how changes in nutrition can regulate Plin2 in liver.