Partitioning of Nutrients During Pregnancy and Lactation: A Review of Mechanisms Involving Homeostasis and Homeorhesis

Lactational Responses to Postruminal Administration of Proteins and Amino Acids

Thyrotropin-releasing hormone (TRH), a hypothalamic tripeptide, binds rapidly and reversibly to specific membrane receptors on GH3 cells, a clonal strain of rat pituitary cells grown in culture. GH3 cells were incubated for 1-72 hr with unlabeled TRH, washed, and then incubated for 1 hr with [3H]TRH. Under these conditions 80% of any bound, unlabeled TRH exchanges with [3H]TRH in the medium, and the amount of radioactivity bound to the cells gives a measure of the number of TRH receptors. In GH3 cells, the number of available TRH receptors decreased from 92% of control after 1 hr to 35% after 48 or 72 hr of incubation with unlabeled TRH. Binding of [3H]TRH to both intact control and TRH-treated cells was half-maximal at 8 nM [3H]TRH, but the maximum amount of [3H]TRH bound was decreased by 75% in cells previously incubated for 48 hr with unlabeled TRH. Equilibrium binding studies were performed using membrane fractions prepared from control cells and cells previously exposed to TRH for various periods. The dissociation constant of the TRH-receptor complex was the same in all cases, but the maximum amount of TRH bound decreased progressively in membrane fractions from cells incubated with TRH for 1-51 hr. TRH receptors were not found in cytoplasmic fractions of control or TRH-treated cells. The loss of TRH receptors was reversible within 4 days. In the continued presence of the tripeptide the number of receptors remained low for 12 days. After incubation for 2 days with different concentrations of TRH, the number of receptors was decreased to 33% of control at 100-300 nM TRH, and half of this decrease occurred at about 1 nM TRH; half-maximal biological responses occur at 2 nM TRH. The biologically active Ntau-methylhistidyl derivative of TRH also effected a loss of receptors, while three inactive analogs of TRH did not cause reductions in the number of TRH receptors. In cultures incubated for 40 hr with cycloheximide, protein synthesis was inhibited by 85%, but the number of TRH receptors was 76% of control suggesting that the receptor has a long half-life. When GH3 cells were incubated with cycloheximide plus TRH, the number of TRH receptors decreased by only 23% as compared to a decrease of 73% in cells incubated with TRH alone, suggesting that receptor loss is partially dependent on active protein synthesis. We conclude that in GH3 cells TRH regulates the number of its own receptors.

Thyrotropin-releasing hormone regulates the number of its own receptors in the GH3 strain of pituitary cells in culture

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Hormonal Control of Lactation

Effect of chronic growth hormone treatment on responses to epinephrine and thyrotropin-releasing hormone in lactating cows.

Preliminary experiments utilizing lactating cows and dairy bulls demonstrated release of prolactin by a single iv injection of 100 Mg synthetic thyrotropin—releasing hormone (TRH). Thereafter, a second experiment described more completely the endocrine changes occurring in the bovine after TRH. Twenty—five, 50 or 100 μg synthetic TRH was administered via jugular cannulae to each of four lactating cows. Serum prolactin immediately before TRH averaged 3.4 ng/ml. Prolactin averaged 21.1, 9.2 and 23.9 ng/ml at 2 min after 25, 50 or 100 μg TRH, respectively. Comparable values at the prolactin peak were 68.0, 23.4 and 60.6 and intervals to the prolactin peak were 10, 8 and 8 min, respectively. Serum prolactin increased in each cow after each dose of TRH, and returned to baseline within 2 hr. Serum thyroxine (μg/100 ml) increased linearly (p < 0.01) for 5 hr, but the increase was not linearly related to dose of TRH. In contrast, growth hormone increased proportionally to the dose of TRH. Total serum glucocortico...

Bovine prolactin, growth hormone, thyroxine and corticoid response to thyrotropin releasing hormone.

Ten lactating Holstein cows were randomly assigned to receive, on 2 consecutive days, either 80 mg ergocryptine (Sandoz-Basel) in 50% ethanol, or 50% ethanol alone. On the day before treatment, serum

Bovine serum prolactin, growth hormone, cortisol and milk yield after ergocryptine.

The response of the mammary gland of rats to various hormones injected daily between days 16 and 32 of lactation was studied. One unit of oxytocin, given 3 times daily, resulted in 37 and 44 % more mammary DNA and RNA content to day 32 of lactation than in saline-injected controls; however, oxytocin did not significantly increase litter weight gain or mammary RNA/DNA ratio. Cumulative litter weight gain decreased markedly in both oxytocin and saline injected rats as lactation advanced. Consequently, the endogenous supply of oxytocin appeared to be sufficient for removal of the reduced amounts of milk synthesized during advanced lactation. Cortisol-21-acetate (0.5 mg), ovine prolactin (2 mg) and ovine growth hormone (1 mg) were injected singularly and in all possible combinations between days 16 and 32 to determine if these treatments would maintain mammary nucleic acid content and lactational performance. Cortisol-21-acetate maintained mammary DNA and RNA content to day 32 of lactation and markedly retard...

Lactational Performance of Rats Injected with Oxytocin, Cortisol-21-acetate, Prolactin and Growth Hormone During Prolonged Lactation

In rats, the influence of pregnancy, fetuses, fetal placentas and pseudopregnancy with and without deciduomas on mammary and uterine development (DNA content) and metabolism (RNA content) was studied. Mammary nucleic acid content increased throughout pregnancy. Removal of fetuses before midpregnancy, but not after, interfered with normal increases in mammary DNA and RNA content. Excision of fetal placentas caused mammary development to regress to nonpregnant control values. Mammary development during the first 12 days of pseudopregnancy was 29–33% less than that observed in 12-day pregnant rats. It is suggested that maternal hormones are the primary stimulant of mammary development during the first half of pregnancy. However, the fetal placentas commence to stimulate mammary development before midpregnancy, and they may be the primary limiting factor for mammary development during the second half of pregnancy. Uterine DNA increased 2.8-fold, whereas uterine RNA and weight increased 5.8- and 4.6-fold, resp...

H. A. Tucker

Papers

Bovine prolactin, growth hormone, thyroxine and corticoid response to thyrotropin releasing hormone.

Bovine serum prolactin, growth hormone, cortisol and milk yield after ergocryptine.

Lactational Performance of Rats Injected with Oxytocin, Cortisol-21-acetate, Prolactin and Growth Hormone During Prolonged Lactation

Contribution of pregnancy, fetuses, fetal placentas and deciduomas to mammary gland and uterine development.