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Hormonal control of α-lactalbumin secretion was studied in mammary tissue obtained from nonlactating multiparous Holstein cows pregnant approximately 8 months. Mammary explants were incubated for 72 h in medium containing insulin, T3 and various combinations or concentrations of PRL, cortisol, progesterone, 17β-estradiol, and GH. Concentrations ofα-lactalbumin in the medium and in homogenates of tissue were measured by RIA or sodium dodecyl sulfate-gel electrophoresis as an index of lactogenesis. Increasing quantities of PRL (25 to 100 ng/ml) progressively increased the release of α-lactalbumin into the medium, whereas concentrations of α-lactalbumin in explants exposed to PRL were similar to those in controls. Mammary explants exposed for 3 h to [3H]leucine plus PRL incorporated approximately 2, 11, and 18 times more label into α-lactalbumin 21–24, 45–48, and 69–72 h after initiation of culture, respectively, than explants cultured in the absence of PRL. Cortisol alone had no effect on α-lactalbumin secretion. However, the addition of PRL into medium containing cortisol increased α-lactalbumin secretion 2.4-fold over that of explants receiving PRL alone and 6.7-fold over that of explants receiving cortisol alone or control explants. Progesterone aloneincreased the secretion of α-lactalbumin approximately 2-fold over that in controls, but decreased PRL-induced α-lactalbumin secretion. 17β-Estradiol alone increased a-lactalbumin secretion over that in control explants and synergized with PRL to increase α-lactalbumin secretion. The addition of progesterone dramatically reduced the synergism between 17β-estradiol and PRL. GH had little effect on α-lactalbumin secretion. We conclude that PRL induces the synthesis and release of α-lactalbumin from mammary explantp of periparturient cows, and that cortisol and 17β-estradiol potentiate the lactogenic effects of PRL, provided progesterone is absent.
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Goodman et al. (1983) studied this question.
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