Search Results
You are looking at 1 - 3 of 3 items for
- Author: D. F. Curran x
- Refine by access: All content x
Search for other papers by J C Byatt in
Google Scholar
PubMed
Search for other papers by P J Eppard in
Google Scholar
PubMed
Search for other papers by J J Veenhuizen in
Google Scholar
PubMed
Search for other papers by T L Curran in
Google Scholar
PubMed
Search for other papers by D F Curran in
Google Scholar
PubMed
Search for other papers by M F McGrath in
Google Scholar
PubMed
Search for other papers by R J Collier in
Google Scholar
PubMed
Abstract
A model of induced lactation was modified to examine the effects of bovine prolactin (bPRL) and bovine placental lactogen (bPL) on mammary growth and differentiation. Thirty-two peripubertal, non-pregnant Holstein heifers were given daily s.c. injections of oestradiol (0·05 mg/kg) and progesterone (0·25 mg/kg) for 7 days to initiate mammary growth. Treatment with bromocriptine (40 mg/3 days) reduced serum PRL concentrations to approximately 25% of pretreatment levels, for the duration of the study. On the day following the last steroid injection, groups of eight heifers were given twice daily s.c. injections of either saline (negative control), recombinant bPRL (rbPRL; 80 mg/day) or recombinant bPL (rbPL; 80 and 160 mg/day) for 7 days. At the end of this period (day 15), growth and differentiation of the mammary glands were assessed. Treatment with rbPL increased total mammary DNA above control value by 50 and 60% for the 80 and 160 mg/day doses respectively. However, total DNA was not different for the control and rbPRL-treated groups. The blood serum concentration of α-lactalbumin was measured daily throughout the study and used as an index of mammary differentiation. Both rbPRL and rbPL stimulated mammary differentiation (i.e. induction of milk synthesis), although rbPRL appeared to be more potent than rbPL. These results indicate that rbPL is lactogenic in vivo and strongly suggest that bPL is a mammary mitogen.
Journal of Endocrinology (1994) 140, 33–43
Search for other papers by J. C. Byatt in
Google Scholar
PubMed
Search for other papers by N. R. Staten in
Google Scholar
PubMed
Search for other papers by J. J. Schmuke in
Google Scholar
PubMed
Search for other papers by F. C. Buonomo in
Google Scholar
PubMed
Search for other papers by S. S. Galosy in
Google Scholar
PubMed
Search for other papers by D. F. Curran in
Google Scholar
PubMed
Search for other papers by G. G. Krivi in
Google Scholar
PubMed
Search for other papers by R. J. Collier in
Google Scholar
PubMed
ABSTRACT
Mature female rats (200 g) were treated for 10 days with either recombinant bovine GH (bGH) or recombinant bovine placental lactogen (bPL) to compare the somatogenic responses elicited by these hormones. The treatments were administered by daily s.c. injection at four dose levels (0·19, 0·56, 1·67 and 5·0 mg/day). Both bGH and bPL stimulated significant increases in weight gain, but the slopes of the dose–response curves were different (P<0·05). Bovine PL was more potent than bGH (P<0·01) at the lowest dose, although there were no differences between treatment groups at the three higher doses. Feed consumption was stimulated more by bPL than bGH at all doses (P<0·001). The concentration of insulin-like growth factor-I (IGF-I) in blood plasma was increased by bGH in a dose-responsive manner and was higher than control at doses of 1·67 and 5 mg/day (P<0·05). Low doses of bPL stimulated increases in IGF-I similar to those with bGH. At the highest dose of bPL, however, there was no concomitant increase in plasma IGF-I. Nevertheless, the growth rate of the animals in this group matched that of the group given the highest dose of bGH. Receptor binding studies indicated that bPL bound to both GH and prolactin receptors. This is consistent with the growth data which suggest that bPL stimulated weight gain through a somatogenic mechanism as well as by another route, possibly mediated by lactogenic receptors.
Journal of Endocrinology (1991) 130, 11–19
Search for other papers by J. C. Byatt in
Google Scholar
PubMed
Search for other papers by P. J. Eppard in
Google Scholar
PubMed
Search for other papers by J. J. Veenhuizen in
Google Scholar
PubMed
Search for other papers by R. H. Sorbet in
Google Scholar
PubMed
Search for other papers by F. C. Buonomo in
Google Scholar
PubMed
Search for other papers by D. F. Curran in
Google Scholar
PubMed
Search for other papers by R. J. Collier in
Google Scholar
PubMed
ABSTRACT
The clearance rate of recombinant bovine placental lactogen (rbPL) from the blood serum of four lactating dairy cows was measured using a specific radioimmunoassay. Two animals were non-pregnant, while the other two were at approximately 120 days of gestation. The rbPL was administered as an i.v. bolus injection (4 mg total) via an indwelling jugular catheter. Blood samples were taken periodically for 180 min and assayed for rbPL. Analysis of the clearance curves for the bolus injection suggested a single-compartment model and a serum half-life of 7·25 min. In a second experiment with the same animals, following cessation of lactation, rbPL or bovine GH (bGH) were administered by s.c. injection (50 mg/day) for 5 consecutive days. Blood samples were taken twice per day during the treatment period and a 3-day pretreatment period. Samples were analysed for glucose, blood urea nitrogen (BUN), non-esterified fatty acids (NEFA), creatinine, insulin, insulin-like growth factor-I (IGF-I) and IGF-II, tri-iodothyronine (T3), progesterone and IGF-binding protein-2 (IGFBP-2) to determine whether rbPL mediates similar metabolic effects to those of bGH. Administration of bGH stimulated an increase in NEFA, glucose, T3 and insulin, whereas none of these variables was affected by rbPL. The plasma concentrations of IGF-I and IGF-II were both increased by treatment with rbPL but, to a lesser extent than occurred with bGH. Interestingly, BUN and IGFBP-2 concentrations were reduced equally by bGH and rbPL. These results suggest that rbPL does not necessarily act as a GH agonist but, rather, may have distinct effects on intermediary metabolism that could be mediated through another specific receptor.
Journal of Endocrinology (1992) 132, 185–193