PS12-12. Maternal Metabolic and Performance Responses to Guanidinoacetic Acid During Late Gestation.

Abstract

This study evaluated the effects of guanidinoacetic acid (GAA) supplementation, with or without rumen-protected methionine (RP-Met), on maternal performance, metabolic responses, and uteroplacental vascular indicators in beef cows. Thirty-six pregnant Nellore cows (initial BW = 502 ± 12.8 kg), each carrying a female fetus, were assigned from day 202 of gestation until calving to one of four treatments in a 2 × 2 factorial arrangement: 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 plus 0.02 g/kg BW RP-Met). Data were analyzed using mixed models (PROC GLIMMIX, SAS), including fixed effects of GAA, RP-Met, and their interaction. No GAA × RP-Met interaction was detected for nutrient intake or performance variables (P > 0.05), and neither supplement affected intake of dry matter, organic matter, crude protein, neutral detergent fiber, or total digestible nutrients (P > 0.05). However, GAA supplementation increased final body weight, average daily gain, shrunk body weight gain, and estimated empty body weight gain (P ≤ 0.02), whereas RP-Met had no effect on performance (P > 0.05). No interaction between GAA and RP-Met was observed for placental measurements (P > 0.05). Control cows exhibited a greater uterine artery pulsatility index compared with cows supplemented with GAA or GAA + RP-Met, with intermediate responses for RP-Met (P = 0.04), while placental weight and cotyledon number were not affected (P > 0.05). Supplementation with GAA, regardless of RP-Met inclusion, increased plasma arginine, citrulline, and ornithine concentrations (P ≤ 0.05), whereas 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 (P > 0.05). Additionally, GAA supplementation reduced the urinary 3-methylhistidine:creatinine ratio (P = 0.01), indicating reduced skeletal muscle protein mobilization, and decreased hepatic arginine:glycine amidinotransferase abundance (P = 0.03), whereas guanidinoacetate N-methyltransferase abundance was not affected. In summary, GAA supplementation during late gestation improved maternal performance, enhanced amino acid availability, reduced muscle protein mobilization, and altered uteroplacental vascular dynamics without affecting nutrient intake, whereas the lack of additive responses to RP-Met suggests that the primary physiological effects of GAA are associated with arginine-sparing and creatine-related metabolic pathways rather than methyl group limitation.

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