Doctor of Philosophy / Department of Animal Sciences and Industry / Barry J. Bradford / The mechanisms behind the metabolic changes observed when transition cows are administered monensin, as well as the effects of supplementing mid-lactation cows with two commercial amino acid products were investigated. Traditionally, the effects of monensin are attributed to increased gluconeogenic precursor supply, but recent research indicated that the effects of monensin extend beyond gluconeogenic flux. Thus, the primary objectives of Experiment 1 were to determine if monensin modulates transition cow feeding behavior, ruminal pH, and/or expression of key metabolic genes. Overall, monensin decreased time between meals prepartum (126 vs. 143 ± 5.0 min; P < 0.03) with a trend appearing postpartum (81.4 vs. 88.8 ± 2.9 min; P < 0.08), which could be related to the smaller ruminal pH standard deviation during the first day cows received the lactation ration (0.31 vs. 0.26 ± 0.015; P < 0.02). Monensin also increased liver mRNA abundance of carnitine palmitoyltransferase 1a (0.15 vs. 0.10 ± 0.002 arbitrary units; P < 0.04), which corresponded to a slower rate of liver triglyceride (TG) accumulation from 7 days before calving through 7 days post calving (412 vs. 128 ± 83 mg TG/g protein over this time period; P = 0.03). No significant effects of monensin supplementation were observed on other metabolic parameters or milk production. Overall, these results confirm that the effects of monensin on transition cows extend beyond altered propionate flux. In Experiment 2, mid-lactation cows consuming a control diet containing 26% wet corn gluten feed (dry matter basis) were compared to cows consuming the same diet supplemented with lysine embedded within Ca salts of fatty acids and the isopropyl ester of 2-hydroxy-4-(methylthio) butanoic acid, a methionine precursor. This trial was conducted because the NRC (2001) model indicated a lysine deficiency prior to supplementation; however amino acid supplementation had no effects. This trial was then extended to decrease dietary CP from 17.9% to 17.1%, and further increase lysine and methionine supply in the treatment diet. No production or intake effects were observed during this period, but MUN was decreased in the treated group (10.8 vs. 12.5 ± 0.2 mg/dL; P < 0.001).