Termination of pregnancy after accelerated lactation in the rat. IV. Relationship to 20alpha-hydroxysteroid dehydrogenase activity and plasma progesterone concentration.

The activity of 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) was assayed in the ovaries of rats after accelerated lactation to determine its relationship to the decrease in progesteron secretion that occurs. When rats were sjbjected to accelerated lactation on Day 9 of pregnancy, activity of the enzyme was only slightly increased by Day 10, but had risen to twice the control level by Day 11, and three times the control level by Day 12. Administration of LH or progesterone prevented the increase in enzyme activity. Progesterone concentration had decreased considerably before the time at which any significant increase in 20alpha-HSD activity was detected. These findings are discussed in relation to the role of 20alpha-HSF in regulating progesterone levels in the rat.     

Adaptation of the small intestine during pregnancy and lactation in the rat.

During pregnancy and lactation in the rat the small intestine in general and the mucosal epithelium in particular gain weight. The specific activities of sucrase, lactate dehydrogenase and succinate-tetrazolium reductase remain constant and those of glucose 6-phosphate dehydrogenase and isocitrate dehydrogenase increase. There is no evidence that the reported decrease in absorption per unit area or weight of mucosal epithelium during pregnancy and lactation is due to decreases in enzyme activities within the epithelium. The pattern of enzyme change shows that the response of the gut to the stimuli of pregnancy and lactation must be a complex one, possibly involving increases in the specific activities of some enzymes.     

Termination of pregnancy after accelerated lactation in the rat. II. Relationship to number of young, day of pregnancy and length of nursing.

Pregnancy is terminated in rats that have mated at the postpartum oestrus if they are allowed to suckle a large litter after implantation. For consistent termination, the number of sucking young must be at least nine, the accelerated lactation must be begun before Day 10 of pregnancy, and must be continued for at least 2 days.     

Prolactin binding in rat mammary gland during pregnancy and lactation.

Lactogenic hormones from the placenta and pituitary are primarily responsible for the growth and function of the mammary gland during pregnancy and lactation. In the present study we described the optimal conditions for the measurement of 125I-labeled ovine prolactin binding to mammary gland slices of pregnant and lactating rats. Prolactin binding is saturable (Kd approx. 2.36 - 10(-9) M), hormone specific and destroyed by proteases. The hormonal environments of pregnancy and lactation dramatically influence the availability and measurement of prolactin binding sites. Whereas binding consistently appears to be low in mammary glands removed from rats during pregnancy, binding levels rise 7--8-fold shortly after birth and remain high during the 22 days of lactation. However, the removal of the ovaries and gravid uteri at specific times during pregnancy results in a prompt 3--6-fold increase in prolactin binding. Elevated levels in potential prolactin binding capacity appear in mammary tissue coincident with the reported rise in serum rat placental lactogen between the eighth and eleventh days. We suggest that high levels of this lactogenic hormone promote the appearance of prolactin binding sites during pregnancy and mask the sites such that they are not available for measurement in vitro.     

Adenosine and the control of lipolysis in rat adipocytes during pregnancy and lactation.

The rate of noradrenaline-stimulated lipolysis is lower in fat-cells from lactating than from pregnant rats; this difference is eliminated by the addition of adenosine deaminase [Aitchison, Clegg & Vernon (1982) Biochem. J. 202, 243-247]. The activity of 5'-nucleotidase, and hence the capacity of the cells to synthesize adenosine, was the same in fat-cells and also stromal cells of adipose tissue from pregnant, lactating and male rats. The response and sensitivity of fat-cells to the anti-lipolytic effects of adenosine were measured by incubating cells in the presence of noradrenaline, adenosine deaminase (to remove endogenous adenosine) and various concentrations of the adenosine analogue N6-phenylisopropyladenosine (PIA). PIA caused a greater inhibition of the rate of noradrenaline-stimulated lipolysis in adipocytes from lactating than from pregnant rats. The concentration of PIA required to inhibit by 50% the rate of noradrenaline-stimulated lipolysis fell from over 100 nM for fat-cells from pregnant rats to 30 nM for fat-cells from lactating rats. The decreased rate of noradrenaline-stimulated lipolysis during lactation was not due to the smaller mean cell volume of adipocytes during this state.