Net absorption and liver metabolism of amino acids and heat production of portal-drained viscera and liver in multiparous sows during transition and lactation

Abstract

Abstract Background Determination of nutrient requirements in the late gestating and lactating sows is essential to optimize sow productivity. The objectives of the present study were to quantify amino acid (AA) fluxes and heat production across portal-drained viscera (PDV) and liver in multiparous sows during transition and lactation. Methods Eight second parity sows were fitted with indwelling catheters in the femoral artery and in the mesenteric, portal and hepatic veins. Eight hourly sets of blood samples were taken starting 0.5 h before feeding at − 10, − 3, + 3, and + 17 d in milk (DIM). Blood gases, plasma metabolites and apparent total tract digestibility (ATTD) of nutrients were measured. Results Feed intake, the ATTD of DM, energy, nitrogen, fat and crude fiber changed with DIM (P < 0.001). Except for Glu, O2, and urea, all net portal fluxes were positive, and all were affected by DIM (P < 0.05) and by sampling time (P < 0.01). Compared with pre partum levels, net portal uptake of AA was 3-63% lower at + 3 DIM but 40-100% higher at + 17 DIM. Net portal fluxes of AA peaked at 1.5 to 2.5 h after feeding except for Glu, and they were positively correlated with changes in sow feed intake across DIM. The net portal recovery was low for Met (49%), Thr (54%), and His (54%) and high for the remaining essential AA (63-69%) and none of them differed across DIM. Net hepatic uptake (i.e. hepatic oxidation) of Lys, Thr, Ile, Leu and Phe peaked at 0.5 to 2.5 h after feeding, whereas uptake of Trp, Val, and His was constant, while that of Met was close to zero. Conclusion The net portal recovery was substantially lower for Met, Thr, and His than the remaining essential AA. Hepatic AA oxidation peaks 0.5 to 2.5 h after feeding. The heat production in PDV and liver was approximately two-fold higher at peak lactation compared to other stages. The study suggests that lysine was the limiting AA in peak lactation but not in early lactation.