Essential AA can activate mTOR signaling and elicit effects on cellular mechanisms controlling protein and lipid metabolism. During gestation the fetus relies almost exclusively on nutrients from the dam, hence, we hypothesized that increasing Met supply to the cow during late-pregnancy alters expression of nutrient transporters and mTOR signaling genes in the placentome leading to differences in calf birth weight. Multiparous cows were fed during the last 28 d of pregnancy with a control or Met-supplemented (Mepron, Evonik Nutrition & Care GmbH, Germany) diet. Mepron was supplied at a rate of 0.09% of DM to ensure a ratio of Lys to Met close to 2.8:1 in the metabolizable protein. Placentome samples were collected from 15 cows per treatment and mRNA expression of 41 genes analyzed using qPCR. Calves from Met-supplemented cows had greater body weight at birth (P = 0.04). MTOR and RPS6KB1 (ribosomal protein S6 kinase β-1) were upregulated (P ≤ 0.07) in Met-fed cows. Met-fed cows also had upregulated 5 neutral AA transporters (P ≤ 0.09; SLC3A2, SLC7A5, SLC38A1, SLC38A2, and SLC38A10), while it downregulated (P = 0.05) SLC43A2. Among the facilitated glucose transporters, Met upregulated (P ≤ 0.07) the expression of SLC2A1, SLC2A3, and SLC2A4, and downregulated SLC2A8 (P = 0.07). In Met-supplemented cows the long-chain fatty acid transporter SLC27A1 and the betaine transporter SLC6A12 were downregulated (P = 0.06), while the multivitamin cotransporter SLC5A6 was upregulated (P = 0.09). Other genes analyzed related to transport of AA (SLC1A1, SLC1A5, SLC6A6, SLC7A8, SLC38A6, SLC38A7), glucose (SLC2A5, SLC2A6, SLC2A9, SLC2A10, SLC2A11, SLC2A12, SLC2A13, SLC5A11), fatty acid (SLC27A2, SLC27A3), vitamin (SLC19A2, SLC19A3, SLC44A1, SLC44A3), and mTOR signaling (AKT1, EIF4EBP1, EIF4EBP2, EEF1A1, ELF2, IRS1) were not affected by Met supply. Overall, our findings indicate that Met supply during late-gestation could enhance utero-placental transport of essential and non-essential AA, glucose and vitamins. As such, differences in body weight at birth in calves from Met-supplemented cows is, at least in part, a result of upregulation of nutrient transporters some of which are controlled by mTOR signaling.