Stimulation of body weight gain of the mature female rat by bovine GH and bovine placental lactogen

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, 0·5...

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Published inJournal of endocrinology Vol. 130; no. 1; pp. 11 - 19
Main Authors BYATT, J. C, STATEN, N. R, SCHMUKE, J. J, BUONOMO, F. C, GALOSY, S. S, CURRAN, D. F, KRIVI, G. G, COLLIER, R. J
Format Journal Article
LanguageEnglish
Published Colchester BioScientifica 01.07.1991
Portland Press
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Summary: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
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ISSN:0022-0795
1479-6805
DOI:10.1677/joe.0.1300011