Leptin and leptin receptor expression in skeletal muscle and adipose tissue in response to in vivo porcine somatotropin treatment.
The present study was performed to examine the response of leptin and leptin receptor (Rb) genes 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 (as-fed basis). At 90 kg, six pigs were treated with daily injections of recombinant pST (10 mg) in sterile bicarbonate buffer, whereas the other six pigs were injected with sterile bicarbonate buffer (controls). With initiation of pST treatment, the quantity of feed offered was 85% of calculated ad libitum intake based on BW and adjusted every 3 d. Diet restriction was designed to correct for the effects of the known inhibition in feed intake because of pST treatment in swine. Animals were maintained on treatment for 2 wk. A blood sample was obtained from each pig on d 14 of treatment, 6 h after pST injection. Tissue samples were collected on d 15, frozen in liquid N2, and stored at -80 degrees C before analysis for mRNA abundance. Total RNA was amplified by reverse transcription (RT) PCR with 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 (LF), liver, latissimus dorsi (LD), and biceps femoris (BF). Restricted feeding resulted in no change in BW of control pigs, whereas pST treatment increased BW by 6.9 +/- 0.5 kg (P < 0.001). Treatment with pST produced a 12-fold increase in serum ST concentration relative to control pigs (P < 0.002). Serum leptin concentration was increased by 17% in swine treated with pST relative to control pigs (P < 0.011). Leptin mRNA abundance was increased in liver by pST treatment (P < 0.05). Administration of pST decreased leptin Rb (Ob-Rb) mRNA abundance by 27% in liver (P < 0.044) and by 49.5% in OSQ (P < 0.025) relative to controls. The present data suggest that pST does not affect leptin expression independent of dietary intake because the restricted feeding regimen used in the present study precluded detection of major change in leptin gene expression. Changes in Ob-Rb mRNA abundance by pST treatment indicate that ST or the metabolic adaptations to ST have a role in regulating Ob-Rb expression.
Ramsay
T G
TG
Growth Biology Laboratory, USDA-ARS, Beltsville, MD 20705, USA. tramsay@anri.barc.usda.gov
Richards
M P
MP
D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D005260:Female; D005508:Food Deprivation; D005786:Gene Expression Regulation / Q000187:drug effects*; D013006:Growth Hormone / Q000494:pharmacology*; D020738:Leptin / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D054411:Receptors, Leptin; D013552:Swine / Q000378:metabolism*
D020738:Leptin; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D013006:Growth Hormone