Our long-term hypothesis is that anaplerosis of the tricarboxylic acid cycle (TCA) by propionate stimulates hepatic oxidation of acetyl CoA, increasing hepatic energy charge and satiety. The objective of this study was to determine the short-term effects of propionate on liver metabolism in dairy cows relative to meals. Eight dairy cows (5–14 DIM) were used in a duplicated 4x4 Latin square design with a 2 × 2 factorial arrangement of treatments. Cows received a pulse dose to the rumen of 1.5 moles of propionic acid (PA) in a 500 mL solution or 500 mL of water (control; CON) either 1 h before or 2 h after feeding. Liver samples were collected before dosing and 10 min post-dosing. Liver samples were analyzed for propionyl CoA (P-CoA), acetyl CoA (A-CoA), fumarate, malate, oxaloacetic acid (OAA) and citrate. Data were analyzed with the Mixed Model option in JMP Pro 13. PA increased malate compared with CON both before (PA: 133 to 267 vs. CON: 162 to 151 nmol/g) and after (PA: 224 to 329 vs. CON: 292 to 227 nmol/g) meals (interaction, P = 0.06). PA tended to increase fumarate compared with CON both before (PA: 39.5 to 57.5 vs. CON: 43.7 to 43.0 nmol/g) and after (PA: 44.1 to 70.2 vs. CON: 55.3 to 54.9 nmol/g) meals (interaction, P = 0.13); likely resulting from the downstream accumulation of malate. OAA was not affected by treatment so conversion of malate to OAA may be a bottleneck for cows in the postpartum period with elevated NADH/NAD. PA tended to increase citrate compared with CON (P = 0.12) and the increase tended to be greater after feeding (PA: 62.0 to 110 vs. CON: 101 to 96.0 nmol/g) than before (PA: 59.4 to 91.9 vs. CON: 51.9 to 58.3 nmol/g; interaction P = 0.12). PA tended to decrease A-CoA compared with CON both before (PA: 8.87 to 5.35 vs. CON: 9.62 to 7.82 nmol/g) and after (PA: 7.84 to 4.04 vs. CON: 4.64 to 6.26 nmol/g) feeding (interaction, P = 0.11). This reduction, along with increased citrate concentration, indicates that anaplerosis from propionate absorption within the timeframe of meals increases TCA cycle activity and likely increases hepatic energy charge despite the potential bottleneck at the malate dehydrogenase reaction.