RESUMEN
Copper is routinely supplemented to weanling pig diets at concentrations above nutritional requirements to enhance growth performance. We hypothesised that this effect depends on the source of Cu and its dietary concentration. We tested this in weaned pigs (26 d of age) over a 35-d period using a 2â¯×â¯3 factorial arrangement with two Cu-sources (CuSO4 and Cu2O, monovalent copper oxide, CoRouge®) and three supplementary dietary Cu-levels (15, 80 and 160â¯mg Cu/kg) as respective factors. Increasing Cu level linearly increased (Pâ¯<â¯0.001) final BW and daily gain. These effects tended (Pâ¯=â¯0.09) to be greater with Cu2O than CuSO4. Feed conversion ratio decreased linearly (Pâ¯<â¯0.001) with increasing dietary Cu content, independent of Cu source. Plasma Cu, Zn and Fe levels were unaffected, whereas liver Cu content increased quadratically (Pâ¯<â¯0.001) with increasing dietary Cu content, with a larger increase (Pâ¯<â¯0.001) with CuSO4 than Cu2O. Bile Cu content increased quadratically (Pâ¯=â¯0.025) with increasing Cu content, irrespective of Cu source. RT-qPCR analysis revealed that increasing Cu content quadratically (Pâ¯=â¯0.009) increased duodenal but not ileal metallothionein 1A (MT1A) mRNA, with greater effect (Pâ¯=â¯0.010) of CuSO4. Regardless of the Cu source, increasing Cu dose linearly increased (Pâ¯=â¯0.006) duodenal DMT1/SLC11A2 mRNA but decreased ZIP4/SLC39A4 mRNA in duodenum (Pâ¯<â¯0.001) and ileum (Pâ¯<â¯0.005). ZnT10/SLC30A10 mRNA was significantly (Pâ¯=â¯0.021) and numerically (Pâ¯=â¯0.061) greater with Cu2O compared to CuSO4, in duodenum and ileum, respectively. Copper content quadratically modulated duodenal but not ileal transferrin receptor (Pâ¯=â¯0.029) and ferric reductase CYBRD1 mRNA (Pâ¯=â¯0.022). In hypothalamus, high Cu dose (Pâ¯=â¯0.024) and Cu2O as source (Pâ¯=â¯0.028) reduced corticotropin-releasing hormone (CRH) mRNA. Low versus high CuSO4 increased corticotropin-releasing hormone receptor (CRHR2) mRNA, while low Cu2O had the opposite effect (Pâ¯=â¯0.009). In conclusion, incremental Cu intake enhanced growth performance, with a tendency for a greater effect of Cu2O. The lower increase in duodenal MT1A mRNA and liver Cu content indicates that less Cu from Cu2O was absorbed by gut and sequestered in liver. Thus, high Cu absorption is not essential for its growth-promoting effect and dietary Cu may affect intestinal Fe and Zn absorption via the active, transcellular route. The effects on hypothalamic CRH and CRHR2 expression indicate a role for the hypothalamus in mediating the effects of Cu on growth performance.