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.