Effects of copper hydroxychloride on growth performance and abundance of genes involved in lipid metabolism of growing pigs

Supplementing Cu to diets fed to pigs at 100 to 250 mg/kg may reduce post-weaning scouring and also improve ADG and ADFI. Addition of Cu at 250 mg/kg in diets for pigs containing 5% animal fat improved growth performance, and it was speculated that this is due to the ability of Cu to improve animal fat utilization and enzymatic activity. Inclusion of 45 mg/kg of dietary Cu in diets for rabbits improved body mass gain by upregulating mRNA transcription of fatty acid transport protein, fatty acid binding protein, and carnitine palmitoyl transferase 1, indicating that dietary Cu may influence post-absorptive metabolism of lipids. However, the effect of supplementing dietary Cu on post-absorptive lipid metabolism in pigs remains inconclusive. Therefore, an experiment was conducted to test the hypothesis that addition of 150 mg/kg Cu from Cu hydroxychloride (IntelliBond CII; Micronutrients USA LLC; Indianapolis, IN) to a diet based on corn, soybean meal (SBM), and distillers dried grains with solubles (DDGS) improves growth performance of pigs, and that dietary Cu influences mRNA abundance of genes involved in post-absorptive metabolism of lipids in pigs.

 

Experimental design

Thirty two pigs (initial BW: 15.0 ± 1.0 kg) were allotted to 2 dietary treatments with 2 pigs per pen for a total of 8 replicate pens per treatment. Pigs were fed a corn-SBM-DDGS control diet that included Cu to meet the requirement. A second diet was formulated by adding 150 mg/kg Cu from Cu hydroxychloride to the control diet. On the last day of the experiment, one pig per pen was sacrificed and samples from liver, skeletal muscle, and subcutaneous adipose tissue were collected to analyze relative mRNA abundance of genes involved in lipid metabolism.

 

Results

Overall ADG and G:F were greater (P < 0.05) for pigs fed the diet containing Cu hydroxychloride compared with pigs fed the control diet (Table 1). Pigs fed the diet supplemented with Cu hydroxychloride also had increased (P < 0.05) abundance of cluster of differentiation 36 in liver and increased (P < 0.05) abundance of fatty acid binding protein 4 and lipoprotein lipase in subcutaneous adipose tissue (Table 2). Inclusion of Cu hydroxychloride also tended to increase (P < 0.10) abundance of fatty acid binding protein 1, peroxisome proliferator-activated receptor alpha, and carnitine palmitoyl transferase 1 B in liver, skeletal muscle, and subcutaneous adipose tissue, respectively.

 

Key points

  • Supplementation of Cu from Cu hydroxychloride to the control diet improved ADG and G:F of pigs.
  • Supplementation of Cu from Cu hydroxychloride the control diet increased mRNA abundance of genes involved in uptake, transport, and oxidation of fatty acids.

 

Table 1. Growth performance for pigs fed diets containing 0 or 150 mg Cu/kg from Cu hydroxychloride1

 

Diet

 

 

Item

Control

Control + Cu2

SEM

P-value

d 0 to 15

   

 

 

  Initial BW, kg

15.150

14.949

0.455

0.132

  ADG, kg

0.578

0.654

0.031

0.070

  ADFI, kg

1.018

1.009

0.038

0.876

  G:F

0.570

0.648

0.027

0.080

  Final BW, kg

23.825

24.757

0.510

0.150

d 15 to 28

 

 

 

 

  ADG, kg

0.827

0.843

0.033

0.747

  ADFI, kg

1.570

1.448

0.048

0.113

  G:F

0.530

0.586

0.028

0.157

 Final BW, kg

34.575

35.713

0.492

0.076

d 0 to 28

 

 

 

 

  ADG, kg

0.694

0.742

0.021

0.037

  ADFI, kg

1.275

1.214

0.033

0.119

  G:F

0.546

0.612

0.018

0.024

s

s

s

s

s

1Data are least squares means of 8 observations per treatment.

2The diet containing added Cu was fortified with 150 mg/kg of Cu from Cu hydroxychloride (IntelliBond CII; Micronutrients USA LLC; Indianapolis, IN).

 

Table 2. Least squares means (log2-backtransformed) for expression of genes in the liver, skeletal muscle, and subcutaneous adipose tissue of pigs fed diets containing 0 or 150 mg Cu/kg from Cu hydroxychloride1

 

 

Diet

 

 

Item2

Control

Control + Cu3

SEM

P-value

Liver

   

 

 

  FAS

0.681

0.926

0.192

0.329

  CD36

0.839

1.094

0.064

0.017

  ACC

0.823

0.886

0.136

0.746

  PPAR-α

0.857

0.923

0.089

0.451

  CPT1A

1.031

1.000

0.078

0.678

  FABP1

0.774

1.137

0.098

0.067

Skeletal muscle

 

 

 

 

  FAS

0.678

1.314

0.315

0.742

  CD36

1.031

1.391

0.219

0.215

  ACC

0.564

0.809

0.245

0.418

  PPAR-α

0.732

0.877

0.046

0.082

  CPT1B

0.877

0.835

0.077

0.682

  FABP3

0.889

0.797

0.062

0.308

  FATP1

0.826

0.687

0.069

0.158

Subcutaneous adipose tissue

  FAS

0.559

0.951

0.334

0.312

  CD36

1.031

1.391

0.219

0.215

  ACC

0.564

0.809

0.245

0.418

  PPAR-α

0.784

0.966

0.119

0.188

  CPT1B

0.960

1.395

0.126

0.075

  FABP4

0.998

1.320

0.149

0.035

  FATP1

1.081

1.159

0.107

0.651

  PPAR-ɤ

1.049

1.396

0.182

0.160

  LPL

0.985

1.462

0.143

0.004

  HSL

0.802

1.135

0.184

0.126

2

2

2

2

2

1Data are least squares means of 7 or 8 observations per treatment.

2FAS = fatty acid synthase; CD36 = cluster of differentiation 36/fatty acid translocase; ACC = acetyl CoA carboxylase;  PPAR-α = peroxisome proliferator-activated receptor alpha; CPT1A = carnitine palmitoyl transferase 1 A; FABP1 = fatty acid binding protein 1; CPT1B = carnitine palmitoyl transferase 1 B; FATP1 = fatty acid transport protein 1; FABP3 = fatty acid binding protein 3; FABP4 = fatty acid binding protein 4; PPAR-ɤ = peroxisome proliferator-activated receptor gamma; LPL = lipoprotein lipase; HSL = hormone sensitive lipase.

3The diet containing added Cu was fortified with 150 mg/kg of Cu from Cu hydroxychloride (IntelliBond CII; Micronutrients USA LLC; Indianapolis, IN).

 

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