Uncoupling protein expression in skeletal muscle and adipose tissue in response to in vivo porcine somatotropin treatment

These experiments examined the potential roles of somatropin (pST) and IGF-I in the regulation of uncoupling protein (UCP)2 and UCP3 and their regulatory proteins peroxisome proliferator activated receptor (PPAR) α, γ and δ using in vivo pST treatment of swine and in vitro supplementation of pST or IGF-I to adipose slices. Six, 90 kg barrows were treated with recombinant pST (10 mg) for 2 week while another six pigs were injected with buffer. Total RNA from outer subcutaneous adipose (OSQ) and middle subcutaneous adipose (MSQ) tissues, leaf fat, liver and longissimus (LM) was amplified by reverse transcription-PCR with quantification of transcripts by capillary electrophoresis with laser-induced fluorescence detection. UCP2 mRNA abundance increased in liver (P < 0.001) and all three adipose tissues by pST treatment (P < 0.05). Administration of pST increased UCP3 mRNA abundance by 42% in LM (P < 0.01). PPARα mRNA abundance increased with pST treatment by 29% in liver (P < 0.05), while decreasing 25% in LM (P < 0.05). PPARγ mRNA abundance decreased 32% (P < 0.01) while PPARδ increased 48% in LM (P < 0.01) with pST administration. In vitro, pST reduced UCP2 mRNA abundance in OSQ and MSQ tissue slices (P < 0.05). UCP3 mRNA abundance decreased in OSQ (P < 0.05) but increased in MSQ (P < 0.05) with pST. In contrast, IGF-I increased UCP2 and UCP3 mRNA abundance in both MSQ and OSQ slices (P < 0.05). These experiments suggest pST, IGF-I and metabolic adaptations to pST contribute to regulating UCP2 and UCP3.