Submitted to: Journal of Animal Physiology and Animal Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/20/2007
Publication Date: 10/1/2008
Citation: Weber, T.E., Kerr, B.J., Spurlock, M.E. 2008. Regulation of hepatic peroxisome proliferator-activated receptor-alpha (PPAR-a) expression but not adiponectin by dietary protein in finishing pigs. Journal of Animal Physiology and Animal Nutrition. 92(5):569-577. Interpretive Summary: Reducing the crude protein content of pig diets has been shown to reduce nitrogen excretion. However, decreasing the amount of soybean meal (to reduce crude protein) in swine diets has been associated with decreased carcass leanness. It has been demonstrated that feeding supplemental leucine to pigs increases the abundance of intramuscular fat. In some species, soy protein regulates adiponectin and peroxisome proliferator activated receptor-alpha (PPAR-a), proteins that regualte fat deposition. The effect of dietary soy protein on adiponectin and PPAR-a in the pig has not been studied. Therefore, an experiment was conducted to determine whether reducing or replacing dietary soybean meal, or adding crystalline leucine influences serum adiponectin, adiponectin mRNA, serum metabolites, and the expression of PPAR-a and other genes involved in lipid deposition. Finishing pigs were subjected to one of four dietary treatments: 1) reduced crude protein diet containing soybean meal 2) high crude protein diet containing soybean meal, 3) high crude protein diet with corn gluten meal replacing soybean meal, and 4) high crude protein diet with soybean meal and crystalline leucine to equal 3% total leucine for 35 days. The type of diet fed had no impact on overall growth performance or predicted carcass lean content, but pigs fed the crystalline leucine had smaller loin eye areas than pigs fed the other treatments. Dietary treatment did not affect adiponectin gene expression or circulating levels. The expression of genes that regulate lipid deposition in adipose tissue or loin muscle was not affected by dietary treatment. In liver tissue, the expression of the PPAR-a gene was reduced in pigs fed reduced levels of soybean meal. Protein analysis revealed that reducing the amount of soybean meal in the diet reduced the abundance of PPAR-a protein in the liver. These findings suggest that mechanisms other than decreasing adiponectin are responsible for decreased leanness found in pigs fed reduced crude protein diets. The research results described in this report provide researchers at universities, feed companies, allied industries, and swine production facilities data showing that reducing or removing soybean meal from pig diets does not alter adiponectin, but does reduce the expression of PPAR-a, a gene that regulates lipid utilization.
Technical Abstract: Dietary soy protein reduction and supplemental leucine (Leu) have been found to decrease leanness and increase muscle lipid content of pig carcasses respectively. Soy protein regulates adiponectin and peroxisome proliferator activated receptor-alpha (PPAR-a) in some species, but the effect of dietary soy protein on adiponectin and PPAR-a in the pig has not been studied. Therefore, the objective of this study was to determine whether soybean meal reduction, replacement or supplemental Leu influences serum adiponectin, adiponectin mRNA, serum metabolites, and the expression of PPAR-a and other genes involved in lipid deposition. Forty-four pigs (11 pigs per treatment) were subjected to one of four dietary treatments: 1) reduced CP diet containing soybean meal (RCP-Soy), 2) high CP diet containing soybean meal (HCP-Soy), 3) high CP diet with corn gluten meal replacing soybean meal (HCP-Corn), and 4) high CP diet with soybean meal and crystalline Leu to equal 3% total Leu (HCP-Leu) for 35 d. Dietary treatment had no effect on overall performance, but pigs fed the HCP-Soy diets had greater G:F (P < 0.05) than all other treatments during wk 2. No effect of dietary treatment was found for 10th rib backfat depth, muscle lipid content or predicted carcass lean percentage, but pigs fed the HCP-Leu diets had smaller (P < 0.05) longissimus muscle areas than pigs fed the other diets. There was no effect of dietary treatment on serum adiponectin or leptin. Dietary treatment did not affect the abundance of the mRNAs for adiponectin, PPAR-a, PPAR-gamma2, lipoprotein lipase, or fatty acid synthetase in subcutaneous adipose tissue. The mRNA expression of PPAR-a, PPAR-gamma2, lipoprotein lipase, or fatty acid synthetase in longissimus muscle was not affected by dietary treatment. In liver tissue, the relative abundance of PPAR-a mRNA was greater (P < 0.05) in pigs fed the HCP-Soy diets as compared to pigs fed RCP-Soy or HCP-Corn diets. Hepatic mRNA expression of fatty acid synthetase was not affected by dietary treatment. Western blot analysis indicated that hepatic PPAR-alpha protein levels were decreased (P < 0.05) in pigs fed the RCP-Soy diets as compared to pigs fed the HCP-Soy diets. These data indicate that dietary soy protein reduction or removal does not regulate adiponectin in the pig. Furthermore, these data suggest that increasing the soy protein content of swine diets increases hepatic expression of PPAR-a without associated changes in body composition.