Evidence for a mammogenic role of growth hormone in ewes: effects of growth hormone-releasing factor during artificial induction of lactation.
Thirty-two 1-yr-old nulliparous Prealpes du Sud ewes were randomly allocated in a 2 x 2 factorial design and induced to lactate by injection of estradiol (.5 mg x kg(-1) x d(-1)) and progesterone (1.25 mg x kg(-1) x d(-1)) for 7 d (d 1 to 7). On d 18, 19, and 20, ewes received 1 mg/kg of hydrocortisone acetate twice daily to induce lactogenesis. Experimental ewes (n = 16) received human growth hormone-releasing factor 1-29 NH2 (hGRF 1-29 NH2) treatment (four daily x 100 microg hGRF i.v.) from d 10 to d 20. The other 16 ewes were controls. Half of both groups was maintained at either 8.5 h (ShD) or 15.5 h light (LD), and half of each subgroup was slaughtered on d 21. The remaining ewes were milked during a 6-wk period. Mammary gland epithelial tissue DNA concentration and liver growth hormone (GH) binding were evaluated on tissues from slaughtered ewes. The estrogen-progesterone treatment induced mammary gland development and enhanced the plasma concentrations of prolactin (PRL), GH, and IGF-I between d 1 and 7; concentrations increased 1.5, 2.3, and 2.6 times, respectively (P = .002). Between d 10 and 20, hGRF treatment enhanced (P < .001) plasma concentrations of GH (5 +/- 1.4 ng/mL on d 7 vs 14.4 +/- 1.3 ng/mL on d 20) and IGF-I (722 +/- 42 ng/mL on d 7 vs 1,281 +/- 82 ng/mL on d 18). Mammary DNA concentration at d 21 was greater (P = .07) for hGRF-treated ewes (1.2 vs .95 mg/g fresh tissue). Milk yield was greater (P < .025) in the hGRF groups (246 +/- 25 g/d vs 128 +/- 40 g/d). The long photoperiod regimen enhanced these responses. These results suggest that mammogenesis and(or) early lactogenesis in ewes is in part controlled by GH.
Kann
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Unité de Recherches sur le Placenta et la Périnatalité, Laboratoire de Biologie Cellulaire et Moléculaire, I.N.R.A., Jouy en Josas, France.
D000818:Animals; D004247:DNA / Q000032:analysis; D004848:Epithelium / Q000737:chemistry / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D013006:Growth Hormone / Q000097:blood / Q000502:physiology*; D013007:Growth Hormone-Releasing Hormone / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000378:metabolism; D007774:Lactation / Q000187:drug effects / Q000502:physiology*; D008099:Liver / Q000737:chemistry; D008321:Mammary Glands, Animal / Q000737:chemistry / Q000502:physiology*; D008892:Milk / Q000378:metabolism; D017440:Photoperiod; D011374:Progesterone / Q000494:pharmacology; D011388:Prolactin / Q000097:blood; D011897:Random Allocation; D011986:Receptors, Somatotropin / Q000032:analysis / Q000187:drug effects; D012756:Sheep / Q000097:blood / Q000378:metabolism / Q000502:physiology*
D011986:Receptors, Somatotropin; D011374:Progesterone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D011388:Prolactin; D013006:Growth Hormone; D004247:DNA; D013007:Growth Hormone-Releasing Hormone; D006854:Hydrocortisone