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1 Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, AB, Canada
* To whom correspondence should be addressed. E-mail: ron.ball{at}ualberta.ca.
We have shown that first-pass intestinal metabolism is necessary for approximately 50% of whole-body arginine synthesis from its major precursor, proline, in neonatal piglets. Further to that, the intestine is not the site of increased arginine synthesis observed during dietary arginine deficiency. Primed, constant intravenous (IV) and intraportal (IP) infusions of L-[U-14C]proline, and IV infusion of either L-[guanido-14C]arginine or L-[4,5-3H]arginine were used to measure first-pass hepatic arginine synthesis in piglets enterally-fed either deficient (0.20 g.kg-1.d-1) or generous (1.80 g.kg-1.d-1) quantities of arginine for 5 days. Conversion of arginine to other urea cycle intermediates and arginine recycling were also calculated for both dietary treatments. Arginine synthesis (g.kg-1.d-1) from proline was greater in piglets (P < 0.05) fed the deficient arginine diet in both the presence (generous: 0.07, deficient: 0.17, pooled SEM = 0.01) and absence (generous: 0.06, deficient: 0.20, pooled SEM = 0.01) of first-pass hepatic metabolism. There was no net arginine synthesis from proline during first-pass hepatic metabolism, regardless of arginine intake. Arginine conversion to urea, citrulline and ornithine were significantly greater (P < 0.05) in piglets fed the generous arginine diet. Calculated arginine fluxes were significantly lower (P = 0.01) for [4,5-3H]arginine than [guanido-14C]arginine, and the discrepancy between the values was greater in piglets fed the deficient arginine diet (35% versus 20%). Collectively, these findings show that first-pass hepatic metabolism is not a site of net arginine synthesis and that piglets conserve dietary arginine in times of deficiency by decreasing hydrolysis and increasing recycling.
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