Two experiments were conducted to evaluate effects of ractopamine (RAC) and steroidal implant treatments on performance, carcass traits, blood metabolites, and lipogenic enzyme activity in feedlot cattle. In Exp. 1, yearling steers (n = 486; initial BW = 305 kg) were used in a 3 × 3 factorial arrangement of RAC doses of 0 (R0), 100 (R100), or 200 (R200) mg·steer(-1)·d(-1) fed for 28 d and implant regimens (implant-reimplant) of no implant-no reimplant (NI-NI), 120 mg of trenbolone acetate (TBA) and 24 mg of estradiol-17β (E17B)-no implant (RS-NI), or 80 mg of TBA and 16 mg of E17B followed by 120 mg of TBA and 24 mg of E17B (RI-RS). Except for KPH and skeletal maturity score, no RAC × implant interactions were noted (P > 0.10). Carcasses from R200 were 6.3 kg (P = 0.042) heavier than those from R0. Marbling, calculated empty body fat (EBF), and USDA quality grade did not differ (P > 0.10) among RAC treatments. The RI-RS steers had 12.6 kg (P = 0.001) and 41.1 kg (P < 0.001) greater HCW than RS-NI and NI-NI, respectively. Despite no difference (P > 0.10) in EBF, marbling score was decreased for RI-RS (P < 0.001) and RS-NI (P = 0.001) relative to NI-NI, resulting in 14.6 and 11.4 percentage unit fewer USDA Prime and Choice carcasses with RI-RS (P = 0.008) and RS-NI (P = 0.039) than with NI-NI. In Exp. 2, heifers (n = 48; initial BW = 347 kg) were used in a 3 × 2 factorial arrangement of RAC doses of 0 (R0) or 250 (R250) mg·heifer(-1)·d(-1) and implant regimens of none (NI), 200 mg of TBA (TO), or 200 mg of TBA and 20 mg of E17B (TE). Blood samples were collected at various times during the feeding period, and subcutaneous adipose samples were collected on d 119. For growth and carcass measurements, no RAC × implant interactions (P > 0.10) were detected. The RAC-supplemented heifers had greater HCW (P < 0.10) with no difference in marbling score. For implant regimens, TE heifers had greater HCW than the NI (P = 0.001) and TO (P = 0.037) heifers. Although EBF did not differ among implant treatments (P > 0.10), TE (P = 0.021) and TO (P = 0.039) had fewer Choice carcasses than NI. Heifers with implants had decreased cortisol and increased IGF-1 and NEFA (P < 0.10) compared with NI heifers. An implant × RAC interaction was detected (P = 0.001) for serum urea nitrogen (SUN), with TE and RAC-supplemented heifers having decreased SUN. These data suggest that the effects of implant and RAC on growth and carcass traits are independent and that USDA quality grade and marbling score can differ significantly among carcasses with similar calculated EBF values.

We have investigated the effects of increasing gestational age, maternal undernutrition or restricted placental growth on prolactin receptor (PRLR) gene expression in perirenal adipose tissue collected from foetal sheep during late gestation (term = 147 d +/- 3 d of gestation). Foetal nutrient supply was reduced by either restriction of placental growth following removal of endometrial caruncles before mating or by reducing maternal feed intake by 50% from 115 d of gestation. Total RNA was extracted from adipose tissue taken from foetal sheep between 90 and 145 d of gestation, and only at 141-145 d in placentally restricted, nutrient restricted and control foetuses. Messenger RNAs encoding the long (PRLR1) and short (PRLR2) forms of the PRLR and glyceraldehyde-phosphate-dehydrogenase (GAPDH) were detected and quantified in a ribonuclease protection assay using an antisense RNA probe complementary to ovine PRLR2 and GAPDH. There was a 7.5-fold increase in the amount of perirenal adipose tissue between 90 and 125 d of gestation, compared with a 1.3-fold increase between 125 and 145 d of gestation. The abundance of mRNA encoding PRLR1 and PRLR2 in perirenal adipose tissue increased 10- and sixfold, respectively, between 90 and 125 d of gestation, and then declined by 145 d of gestation. Both placental restriction and maternal undernutrition significantly reduced foetal adipose tissue deposition. The abundance of PRLR1 but not PRLR2 mRNA was reduced in adipose tissue from the placentally restricted group, where as GAPDH mRNA was three times higher than in controls. In contrast, maternal undernutrition from 115 d of gestation did not affect PRLR1, PRLR2 or GAPDH mRNA expression in foetal adipose tissue. It is concluded that during the period of rapid deposition of perirenal adipose tissue, there is a concomitant increase in PRLR gene expression. This indicates that prolactin may play an important role in the growth and maturation of foetal adipose tissue which occurs before birth.

Leptin, an adipocyte-derived factor, has multiple biological roles including mitogenesis. We investigated the effect of normal development, acute and chronic hyperglycemia and hypoglycemia, and selective acute hyperglycemia, or hyperinsulinemia, on fetal ovine white adipose tissue (WAT) leptin mRNA concentrations. Leptin mRNA amounts expressed as a ratio to the internal control ribosomal S2 mRNA decreased threefold with advancing gestational age (P < 0.05). This gestational decrease was opposite to the 10-fold increase in fetal body weight during the same developmental period. Chronic hyperglycemia with hyperinsulinemia led to no change in WAT leptin mRNA concentrations over a 1- to 10-day duration, but it caused a 40% increase over a 14- to 20-day duration (P < 0.05) along with an increase in fetal body weight (P < 0.05). In contrast, hypoglycemia with hypoinsulinemia, while not affecting WAT leptin mRNA from 1 to 34 days, resulted in a 50% decline over a 36- to 76-day duration along with a decline in fetal body weight (P < 0.05). Acute 24-h studies of selective hyperglycemia with euinsulinemia showed no significant change in WAT leptin mRNA, but in response to selective hyperinsulinemia with euglycemia at 24 h, a twofold increase was observed (P < 0.05). We conclude that fetal WAT leptin mRNA amounts are regulated by fetal development and circulating insulin concentrations. We speculate that chronic in utero metabolic perturbations that alter circulating insulin concentrations affect fetal leptin production that may mediate insulin's influence on fetal growth.

Pregnant pony mares in Group A (n = 4) received i.m. injections at 07:00 and 17:00 h of 0.8 mg bromocriptine/kg body weight 0.75 per day beginning on Day 295 of gestation and continuing until parturition. Group B (n = 4) was treated similarly, but perphenazine was administered orally at 0.375 mg/kg body weight twice a day beginning on Day 305 of gestation and continuing until parturition. Mares in Group C (n = 3) received i.m. injections of saline. Mean plasma prolactin and progesterone concentrations were greater (P less than 0.05) for mares in Group C than in Groups A and B from 295 to 309 days of gestation. From 305 days of gestation, plasma prolactin and progesterone concentrations were greater (P less than 0.05) in Group B and C than in Group A mares. Progesterone and prolactin concentrations increased over this period for Group B and Group C mares, but remained constant in Group A mares. From 10 days pre partum through foaling, mares in Group A had lower progesterone (P less than 0.05) and prolactin (P less than 0.01) concentrations than Group B and C mares. All mares in Group A were agalactic at foaling, while all mares in Groups B and C had normal milk secretion. Gestation was longer (P less than 0.05) in Group A than in Group C mares. In Group A, 2 mares retained the placenta for greater than 3 h, 3 mares had dystocia and all 4 mares had thickened, haemorrhagic placentae.(ABSTRACT TRUNCATED AT 250 WORDS)

The regulation of mRNAs encoding insulin-like growth factor I (IGF-I) and the receptor for growth hormone (GH-R) in ovine luteal tissue by luteotrophic and luteolytic hormones was examined. In Expt 1, ewes were hypophysectomized (HPX) on day 5 of the oestrous cycle and administered saline (S), LH, GH, or LH + GH until day 12 of the oestrous cycle (n = 4 ewes per group). Concentrations of luteal mRNA encoding IGF-I in HPX + S ewes and pituitary-intact ewes at day 5 (n = 4) were approximately 60% (P < 0.05) of those in pituitary-intact ewes at day 12 (n = 4). Treatment of HPX ewes with GH or GH + LH, but not LH alone, increased concentrations of mRNA encoding IGF-I to values similar to those in pituitary-intact ewes at day 12. Hypophysectomy also reduced the mean concentration of mRNA encoding GH-R to approximately 60% (P < 0.05) of the values in pituitary-intact ewes (days 5 or 12). Treatment with LH, but not GH, increased (P < 0.05) concentrations of mRNA encoding GH-R to values observed in pituitary-intact ewes. In Expt 2, prostaglandin F2 alpha (PGF2 alpha; 1 mumole) injected into the ovarian artery on day 11 or day 12 of the oestrous cycle had no effect on luteal concentrations of mRNA for either IGF-I or GH-R. In Expt 3, concentrations of mRNA encoding IGF-I increased (P < 0.05) between days 3 and 6 and remained high for the duration (days 9, 12 and 15) of the oestrous cycle while luteal concentrations of mRNA encoding GH-R did not change. In conclusion, responsiveness of the corpus luteum to GH and luteal synthesis of IGF-I are likely regulators of luteal development and function. However, PGF2 alpha-induced luteolysis was not associated with a decrease in concentrations of mRNAs encoding either IGF-I or GH-R.