Supplementation of guanidinoacetic acid with or without rumen-protected methionine during late gestation affect metabolism and performance of pregnant beef cows

The objective of this study was to assess whether maternal guanidinoacetic acid (GAA) supplementation, with or without rumen-protected methionine (RP-Met), during late gestation affects performance, uteroplacental vascular indicators, and metabolic responses in beef cows. From gestation day 202 until parturition, thirty-six pregnant Nellore cows (502 ± 12.8 kg), each carrying a female fetus, were assigned in a 2 × 2 factorial design: control (no GAA or RP-Met), RP-Met (0.02 g/kg BW), GAA (0.12 g/kg BW), or GAA + RP-Met (0.12 g/kg BW GAA + 0.02 g/kg BW RP-Met). No GAA × RP-Met interaction was detected for nutrient intake or performance variables (P > 0.05), and neither GAA nor RP-Met affected nutrient intake (P > 0.05). However, GAA supplementation increased final body weight (P = 0.01), average daily gain (P = 0.01), shrunk body weight gain (P = 0.01), and estimated empty body weight gain (P = 0.02), whereas RP-Met had no effect on cow performance (P > 0.05). No GAA x RP-Met interaction was observed for placental measurements (P > 0.05). Control cows exhibited a greater uterine artery pulsatility index than cows supplemented with GAA or GAA + RP-Met, with intermediate values for RP-Met (P = 0.04). Neither GAA nor RP-Met affected placental cotyledon number or placental weight (P > 0.05). GAA supplementation, alone or in combination with RP-Met, increased plasma arginine, citrulline, and ornithine concentrations (P ≤ 0.05), while RP-Met increased plasma methionine concentrations (P < 0.01). A GAA × RP-Met interaction was observed for plasma homocysteine, with greater concentrations in cows receiving GAA + RP-Met (P = 0.01). Serum creatine, nitric oxide, and urinary creatinine concentrations were not affected by treatment. Cows supplemented with GAA had lower urinary 3-methylhistidine:creatinine ratio (P = 0.01), indicating reduced skeletal muscle protein mobilization. In the liver, GAA supplementation reduced arginine:glycine amidinotransferase (AGAT) abundance (P = 0.03), whereas guanidinoacetate N-methyltransferase (GAMT) abundance was not affected. In conclusion, GAA supplementation during late gestation improved maternal performance, altered amino acid metabolism, reduced muscle protein mobilization, and modified uteroplacental vascular indicators independent of changes in feed intake. The absence of additive performance responses to RP-Met suggests that the primary physiological effects of GAA were driven by arginine-sparing and creatine-related metabolic mechanisms rather than methyl group limitation.