Effect of amino acids supply in reduced crude protein diets on performance, efficiency of mammary uptake, and transporter gene expression in lactating sows.
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To test the hypothesis that reduction in dietary CP concentration coupled with crystalline AA inclusion increases the efficiency of AA use for milk production, mammary AA arteriovenous concentration differences (A-V), AA transport efficiency (A-V/A 100), and transcript abundance of AA transporters and milk protein genes were determined in lactating sows fed 1 of 3 diets containing 9.5% (Deficient), 13.5% (Ideal), or 17.5% (Standard) CP, with a similar profile of indispensable and dispensable AA. On d 7 and 18, arterial and mammary venous blood and mammary tissue were sampled postfeeding. Transcript abundance of AA transporters b(0,+)AT (SLC7A9), y(+)LAT2 (SLC7A6), ATB(0,+) (SLC6A14), CAT-1 (SLC7A1), and CAT-2b (SLC7A2) and milk protein -casein (CSN2) and LALBA (-lactalbumin) were determined using reverse transcription quantitative PCR. Piglet ADG increased curvilinearly (linear and quadratic, P < 0.03) with increasing percent CP from Deficient to Standard. On d 7, Lys and Arg A-V and transport efficiency increased quadratically (P < 0.05) with increasing percent CP. On d 18, Lys A-V tended to increase (linear, P = 0.08) with increasing percent CP. Increasing CP increased Ile and Val A-V on d 7 (linear, P = 0.05 and P = 0.08, respectively) and Leu and Val on d 18 (linear, P = 0.07 and P = 0.04, respectively). On d 7, plasma concentrations of branched chain AA (BCAA):Lys decreased quadratically (P < 0.05). Expression of genes SLC7A9, SLC7A6, SLC6A14, SLC7A1, SLC7A2, CSN2, and LALBA was unaffected by diet. In conclusion, decreasing the dietary CP from 17.5% to 13.5% with inclusion of crystalline AA did not affect piglet ADG, AA transporter, or milk protein gene expression but increased mammary transport efficiency and A-V of Lys and Arg on d 7 of lactation. This increase was associated with a decrease in plasma concentration of BCAA:Lys, suggesting a competitive mechanism between cationic and BCAA for transport of AA across mammary cells.
