ObjectivesContemporary Holsteins (CH) producing more milk than unselected Holsteins (UH), but they are also more susceptible to lipid disorders, especially hepatic steatosis in early lactation. The objective of this study is to investigate the metabolic events underlying the susceptibility of genetically selected cows to lipid disorders.MethodsSerum and liver samples from periparturient CH and UH cows (n = 12/genotype) were examined by biochemical, metabolomics, and transcriptomic analyses. Serum samples were collected weekly from −5 to + 10 weeks of lactation, and the liver samples were collected on day −14, +3, +14, and + 42 of lactation. Data were analyzed by two-way ANOVA with genotype and time as two factors.ResultsThe postpartum increases of blood serum non-esterified fatty acids (NEFAs) was greater in CH cow. Serum triacylglycerols (TAGs) concentration remained comparable to those of the UH cows but the postpartum accumulation of hepatic TAG was greater in CH than in UH cows. This imbalanced lipidome in CH cows was further reflected by a greater decrease of hepatic phosphatidylcholines (PCs), which are responsible for packaging TAGs into the very-low-density lipoproteins (VLDLs). Hepatic choline content did not differ between UH and CH cows, but less phosphocholine and glycerophosphocholine were present in the liver of CH cows. Transcriptomic analysis indicated that, in the CH cows, the expression of CPT and CEPT genes in the CDP-choline pathway, the major PC biosynthesis pathway, were decreased, while the expression of BHMT and PEMT genes in the minor PC biosynthesis pathway, were increased in early lactation.ConclusionsInadequate hepatic biotransformation of choline to phospholipids contributes to PC deficiency and hepatic steatosis in the CH cow. Efforts to elevate PC synthesis could enhance hepatic VLDL export, reduce hepatic steatosis, and improve metabolic health of high-producing dairy cows in early lactation.Funding SourcesUSDA grant.