<p>This study aimed to investigate the effects of different copper sources (copper sulfate and copper glycinate) on growth performance, trace element metabolism and intestinal stem cell activity in growing pigs. In experiment 1, 30 castrated male pigs (Landrace × Large White; initial body weight of 43.11 ± 1.20&#xa0;kg) were randomly assigned to three treatment groups (<i>n</i> = 10): (1) high-dose CuSO₄ group (150&#xa0;mg/kg Cu as CuSO₄•5&#xa0;H₂O), (2) low-dose CuSO₄ group (20&#xa0;mg/kg Cu as CuSO₄•5&#xa0;H₂O), (3) Cu-Gly group (20&#xa0;mg/kg Cu as copper glycinate). The trial lasted for 30 days. The results showed that pigs fed 20&#xa0;mg/kg Cu as Cu-Gly had final body weight (<i>P</i> = 0.247) and weight gain (<i>P</i> = 0.732) comparable to those fed 150&#xa0;mg/kg Cu as CuSO₄, while exhibiting a significantly improved feed conversion ratio. Additionally, hepatic iron concentration in the Cu-Gly group was significantly higher than in the high-dose CuSO₄ group, whereas renal copper accumulation was lower. Fecal copper excretion in the Cu-Gly group was reduced by 76.38% compared to the high-dose CuSO₄ group(<i>P</i> &lt; 0.0001). In experiment 2, an in vitro porcine small intestinal organoid culture system was employed. Our results indicated that the lower dose of copper markedly improved intestinal organoid budding and stem cell amplification (<i>P</i> &lt; 0.01), and Cu-Gly significantly improved the intestinal organoid surface area and stem cell differentiation (<i>P</i> &lt; 0.001). Simultaneously, the high dose of copper treatment significantly inhibited the minerals transported related gene expression (DMT1, ZIP4, CTR1, ZIP8), but induced the MT1A and MT3 expression in organoids (<i>P</i> &lt; 0.01). Thus, our study finds a relatively effective way to substitute for pharmacological doses of copper, probably via regulating the minerals metabolism and improving the intestinal stem cell proliferation and differentiation.</p>

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Effects of Copper Glycinate Replacing High-Dose Copper Sulfate on Growth Performance, Trace Element Metabolism and Stem Cell Activity in Growing Pigs

  • Xinyi Gao,
  • Shuan Liu,
  • Shoujun Zhang,
  • Zizhong Yang,
  • Xin Liu,
  • Xiaoran Li,
  • Ziyue Bai,
  • Menglong Deng,
  • Jing Wang,
  • Dan Wan

摘要

This study aimed to investigate the effects of different copper sources (copper sulfate and copper glycinate) on growth performance, trace element metabolism and intestinal stem cell activity in growing pigs. In experiment 1, 30 castrated male pigs (Landrace × Large White; initial body weight of 43.11 ± 1.20 kg) were randomly assigned to three treatment groups (n = 10): (1) high-dose CuSO₄ group (150 mg/kg Cu as CuSO₄•5 H₂O), (2) low-dose CuSO₄ group (20 mg/kg Cu as CuSO₄•5 H₂O), (3) Cu-Gly group (20 mg/kg Cu as copper glycinate). The trial lasted for 30 days. The results showed that pigs fed 20 mg/kg Cu as Cu-Gly had final body weight (P = 0.247) and weight gain (P = 0.732) comparable to those fed 150 mg/kg Cu as CuSO₄, while exhibiting a significantly improved feed conversion ratio. Additionally, hepatic iron concentration in the Cu-Gly group was significantly higher than in the high-dose CuSO₄ group, whereas renal copper accumulation was lower. Fecal copper excretion in the Cu-Gly group was reduced by 76.38% compared to the high-dose CuSO₄ group(P < 0.0001). In experiment 2, an in vitro porcine small intestinal organoid culture system was employed. Our results indicated that the lower dose of copper markedly improved intestinal organoid budding and stem cell amplification (P < 0.01), and Cu-Gly significantly improved the intestinal organoid surface area and stem cell differentiation (P < 0.001). Simultaneously, the high dose of copper treatment significantly inhibited the minerals transported related gene expression (DMT1, ZIP4, CTR1, ZIP8), but induced the MT1A and MT3 expression in organoids (P < 0.01). Thus, our study finds a relatively effective way to substitute for pharmacological doses of copper, probably via regulating the minerals metabolism and improving the intestinal stem cell proliferation and differentiation.