Creatine supplementation to total parenteral nutrition increases muscle and organ creatine and lowers liver cholesterol in Yucatan miniature piglets (820.17)

In TPN‐fed pigs, we previously demonstrated that tissue creatine concentrations were proportionate to the IV arginine intake, suggesting that arginine availability limited creatine synthesis. TPN is devoid of creatine, so the requirement must be met entirely by de novo synthesis requiring arginine, glycine and methionine as a methyl donor. L‐arginine:glycine amidinotransferase (AGAT) converts arginine and glycine into guanidinoacetic acid (GAA); GAA is methylated via Guanidinoacetate methyltransferase (GAMT) to form creatine. The addition of creatine to TPN may spare arginine and methionine for protein synthesis and other metabolic processes. Piglets (3‐5 d old, N = 14) were fed complete TPN with (CRE, 0.1 g/kg/d) or without creatine (CON) for 14 d. The CRE group had lower kidney and pancreas AGAT activity and lower plasma GAA concentration (P < 0.01) demonstrating a down‐regulation of creatine biosynthesis. CRE pigs also had greater creatine in plasma, liver, kidney and pancreas (P < 0.01). Total creatine in muscle was also higher in CRE (P = 0.05); however, brain creatine was not affected by treatment. There was no difference in liver weight or triglyceride concentration, but total liver cholesterol was ~50% lower in the CRE piglets compared to CON (P < 0.01). Altered lipid metabolism suggests that creatine may have a role in ameliorating TPN‐induced liver damage. The neonatal brain appears to have priority for creatine when supply is limited, but the addition of creatine to TPN may be necessary to support total body creatine accretion in rapidly growing neonates. Grant Funding Source : Supported by Janeway

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