Influence of porcine somatotropin and the beta-adrenergic agonist ractopamine on lipogenic activity and gene expression in pig adipose tissue
Abstract
Administration of porcine somatotropin (pST) or ractopamine to pigs decreases fat deposition. The present study was conducted to determine the influence of pST and ractopamine on lipogenic activity and gene expression in pig adipose tissue. Porcine ST decreased acetyl-CoA carboxylase (ACC) enzyme activity, protein content and mRNA abundance by 40-60%. Parallel decreases were also found for mRNA abundance of the insulin-responsive glucose transporter (Glut 4), but the effect of pST on basal glucose transporter (Glut 1) was less consistent. Reductions in Glut 1 and Glut 4 mRNA levels were observed in skeletal muscle, however, the responses were less pronounced than in adipose tissue. Neither insulin receptor binding nor insulin receptor mRNA level were affected in adipose tissue, indicating that the effect of pST is mediated via a postreceptor event or independent of insulin action. A portion of the porcine ACC (pACC) and insulin receptor (pIR) cDNAs have been isolated and sequenced with polymerase chain reaction (PCR), in which the pACC is 94% homologous to rat ACC and the pIR is 86% homologous to mouse insulin receptor, respectively. Using reverse-transcriptase PCR, pACC expression was lowest in pST-treated pigs, but pIR expression was not changed. Combined evidence indicates that pST may inhibit fatty acid synthesis in pig adipose tissue by regulating ACC activity at a pretranslational site. Decreased Glut 1 and Glut 4 mRNA suggest that pST may have similar actions on glucose uptake in both adipose and muscle tissues. To determine the effects of ractopamine, the outer and middle subcutaneous fat layers were collected from pigs fed ractopamine (20 mg/kg feed; 2 kg diet/day) for 0, 1, 8 or 24 days. Total and active-state ACC activities were greater in the outer layer, but malic enzyme activity was higher in the middle layer. Ractopamine feeding did not significantly affect total ACC and malic enzyme activities in either layer, and tended to decrease active-state ACC activity by day 8 in both layers. However, the effect on active-state ACC was reversed by day 24. In contrast to ACC activity, ACC mRNA abundance was greater in the middle layer than in the outer layer, and ractopamine had no effect on ACC mRNA level. No differences were found for Glut 1 and Glut 4 mRNA levels between layers, and ractopamine did not alter Glut 1 and Glut 4 mRNA levels. Present results indicate that ractopamine may inhibit lipid synthesis in pig adipose tissue by inactivating ACC enzyme in the short-term. However, minimal responses to ractopamine suggest that adipose tissue may not be the primary target for this agonist in the pig.
Degree
Ph.D.
Advisors
Mills, Purdue University.
Subject Area
Livestock
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