Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 10, 2005
Publication Date: November 1, 2005
Citation: Ramsay, T.G., Richards, M.P. 2005. Leptin and leptin receptor expression in skeletal muscle and adipose tissue in response to in vivo porcine somatotropin treatment. Journal of Animal Science. 83:2501-2508. Interpretive Summary: Leptin is a hormone produced by pig adipose tissue that can affect feeding behavior, animal health and reproduction. Studies in pigs have demonstrated that leptin can reduce feed intake. This study attempted to determine whether expression of leptin and its receptor can be manipulated by hormonal mechanisms in finishing swine by using porcine somatotropin treatment. The data demonstrate that leptin secretion can be stimulated by porcine somatotropin. Secondly, expression of the leptin receptor gene is also responsive to hormonal stimuli in finishing swine. In contrast, the leptin gene does not appear responsive to somatotropin treatment when the effects of pST on depression of feed intake are taken in account. These results suggest the potential to manipulate the efficiency of feeding behavior in finishing animals by altering expression of genes associated with feed intake and metabolism at a time when changes in body composition can be critical for improving profitability.
Technical Abstract: The present study was performed to examine the response of the leptin and leptin receptor gene to porcine somatotropin (pST) stimuli in finishing pigs. Twelve crossbred barrows (Yorkshire x Landrace) were used in this study. Animals were individually fed a basal diet containing 18% CP, 1.2% lysine, and 3.5 Mcal of DE/kg ad libitum. At 90 kg, six randomly selected pigs were treated with daily injections of recombinant pST, (10 mg). The other six pigs were injected with the sterile bicarbonate buffer (controls). With initiation of pST treatment, the amount of feed offered was at 85% of calculated ad libitum intake, based upon BW and adjusted every 3 d. Diet restriction was performed to correct for the effects of the known inhibition in feed intake due to pST treatment in swine. Animals were maintained on treatment for 2 wk. A blood sample was obtained from each pig on the 14th d of treatment at 1500. Tissue samples were collected on d15 and frozen in liquid nitrogen and stored at -80ºC prior to analysis for gene expression by RT-PCR and subsequent quantification of transcripts by capillary electrophoresis with laser-induced fluorescence detection. Samples included outer subcutaneous adipose tissue (OSQ), middle subcutaneous adipose tissue (MSQ), leaf fat, liver, latissimus dorsi (LD) and biceps femoris (BF). Restricted feeding resulted in no change in bwt of control pigs while pST treatment increased bwt by 6.9 ± 0.5 kg (p < 0.001). Treatment with pST produced a twelve-fold increase in serum ST relative to control pigs (p < 0.002). Serum leptin level was elevated by 17% in swine treated with pST relative to control pigs (p < 0.011). Leptin mRNA level was increased in liver by pST treatment (p < 0.05). Leptin receptor (Ob-Rb) expression was inhibited by pST administration by 27% in liver (p < 0.044)and by 49.5% in OSQ (p < 0.025). The present data would suggest that any effect of pST on leptin gene expression in ad libitum fed pigs is primarily the result of pST's inhibition of feed intake, since the restriction feeding regimen used in the present study precluded detection of major change in leptin gene expression. Down regulation of the leptin receptor by in vivo pST treatment implies a reduced sensitivity to leptin in liver and OSQ and perhaps a reduced capacity to inhibit lipogenesis and promote lipolytic activity of the porcine adipocyte in OSQ.