Hormonal control of mammogenesis and onset of lactation in cows--a review

Estrogen stimulates development of mammary ducts, and progesterone and estrogen stimulate proliferation of secretory tissues. In vivo, sequential addition of insulin (step 1), glucocorticoid (step 2), and prolcatin (step 3) leads to biosynthesis of casein and lactose. In cows, mammogenesis continues until termination of pregnancy and overlaps onset of lactation. Progesterone probably inhibits differentiation of secretory cells at step 2 or step 3. Sensitivity of individual cells to progestational inhibition may decrease variably which may be interdependent upon relative increases in estrogen, prolactin, corticoids, and growth hormone to cause asynchronies among them at calving. Since prolactin in plasma is not correlated with progesterone or the estrogens, factors other than feed-back effects of ovarian steroids may be responsible for its sustained increase periparturiently. Also, elevated prolactin periparturiently may be unrelated to subsequent rates of lactation because its "basal" concentrations may meet requirements when inhibiting effects of progesterone are removed. This concept is attractive because mammary cells neither are synchronized highly for biosynthesis nor secrete normal milk for several days after calving. At the latter time, concentrations in plasma are low for progesterone and estrogen, similar to 3 days before calving for glucocoiticoids and prolactin, and increasing for insulin. Evidence of lactation under unusual circumstances was discussed.