The effects of branched-chain amino acid interactions on growth performance, blood metabolites, enzyme kinetics and transcriptomics in weaned pigs

The impact of excess dietary leucine (Leu) was studied in two growth assays with pigs (8–25 kg). In each trial, forty-eight pigs were allotted to one of six dietary groups. The dietary Leu supply increased from treatment L100 to L200 (three increments). To guarantee that interactions between the bra...

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Veröffentlicht in:British journal of nutrition 2010-04, Vol.103 (7), p.964-976
Hauptverfasser: Wiltafsky, Markus Karl, Pfaffl, Michael Walter, Roth, Franz Xaver
Format: Artikel
Sprache:eng
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Zusammenfassung:The impact of excess dietary leucine (Leu) was studied in two growth assays with pigs (8–25 kg). In each trial, forty-eight pigs were allotted to one of six dietary groups. The dietary Leu supply increased from treatment L100 to L200 (three increments). To guarantee that interactions between the branched-chain amino acids (BCAA) were not cushioned either surpluses of isoleucine (Ile, expt 1) or valine (Val; expt 2) were avoided. In the fifth treatment, the effects of a simultaneous excess of Leu and Val (expt 1), or of Leu and Ile (expt 2) were investigated. The sixth treatment was a positive control. An increase in dietary Leu decreased growth performance, and increased plasma Leu and serum α-keto-isocaproate levels in a linear, dose-dependent manner. Levels of plasma Ile and Val, and of serum α-keto-β-methylvalerate and α-keto-isovalerate, indicated increased catabolism. Linear increases in the activity of basal branched-chain α-keto acid dehydrogenase in the liver confirmed these findings. No major alterations occurred in the mRNA of branched-chain amino acid catabolism genes. In liver tissue from expt 2, however, the mRNA levels of growth hormone receptor, insulin-like growth factor acid labile subunit and insulin-like growth factor 1 decreased significantly with increasing dietary Leu. In conclusion, excess dietary Leu increased the catabolism of BCAA mainly through posttranscriptional mechanisms. The impact of excess Leu on the growth hormone–insulin-like growth factor-1 axis requires further investigation.
ISSN:0007-1145
1475-2662
DOI:10.1017/S0007114509992212