Effects of chronic thyroid hormone administration on pregnancy, lactogenesis and lactation in the rat

1992 ◽  
Vol 127 (6) ◽  
pp. 547-554 ◽  
Author(s):  
Roberto R Rosato ◽  
Maria S Gimenez ◽  
Graciela A Jahn

We studied the effects of daily administration of 1 mg/kg thyroxine (T4) starting 10–15 days before mating, on parturition, maternal behavior and lactation in rats. Treated rats had elevated serum titers of T3 and T4, a greater number of fetuses and parturition was advanced approximately 12 h and lasted longer than in controls. None of the treated rats were able to lactate because of defects in maternal behavior and milk ejection; the litters died usually within 48 h postpartum. In rats sacrificed at 10.00 on day 21 of pregnancy, mammary gland content of total protein, phospholipids, casein and lactose were significantly increased, but total lipid was markedly reduced. Lipogenesis was also significantly increased, as well as the activity of the lipogenic enzymes glucose-6-phosphate dehydrogenase, fatty acid synthetase and isocytrate dehydrogenase. These results are indicative of normal albeit premature lactogenesis. The T4-treated rats also had advances in the prepartum fall in serum progesterone and the increase in prolactin as well as in the increase in mammary casein and lactose concentrations of approximately 12 h with respect to control pregnant rats. These results show that chronic T4 treatment induces an advance of approximately 12 h in luteolysis, which in turn advances lactogenesis and parturition in rats. Although the mammary gland was able to produce milk, lactation failed due to abnormal maternal behavior and milk ejection, the causes of which are still unknown. Other effects of hyperthyroidism were also present, such as a severe reduction in lipid content of the gland. The observed increases in lipogenesis and lipogenic enzyme activities could be due to a combination of the effects of hyperthyroidism per se as well as to the increase in lipogenesis that occurs during lactogenesis.

1991 ◽  
Vol 129 (3) ◽  
pp. 343-350 ◽  
Author(s):  
G. A. Jahn ◽  
R. P. Deis

ABSTRACT The part played by the adrenergic system on the release of prolactin and lactogenesis induced by prostaglandin F2α and the antiprogesterone RU 486 was studied in pregnant rats. Two doses of prostaglandin F2α (150 μg) administered at 08.00 and 12.00 h on day 19 of pregnancy induced, at 12.00 h on day 20 (24 h after administration), a significant increase in the serum concentration of prolactin, with a significant decrease in serum progesterone levels. These hormonal changes significantly augmented casein and lactose levels in the mammary gland. Treatment with RU 486 (2 mg/kg) at 08.00 h on day 19 augmented casein and lactose concentrations in the mammary gland at 12.00 h on day 20 without modifying serum concentrations of prolactin and progesterone. The adrenergic antagonists, propranolol (3 mg/kg), metoprolol (10 mg/kg), ICI 118 551 (200 μg/kg), idazoxan (100 μg/kg) and prazosin (10 mg/kg), were administered s.c. at 12.00 and 20.00 h on day 19 and 08.00 h on day 20 of pregnancy to intact rats or to rats previously treated with RU 486 or prostaglandin F2α. These adrenergic antagonists did not modify serum prolactin or progesterone levels in intact or RU 486-treated rats, but serum prolactin levels in the prostaglandin F2α-treated group were significantly reduced by treatment with propranolol, metoprolol or prazosin. In addition, propranolol and ICI 118 551 also decreased the casein and lactose concentrations in the mammary glands of RU 486- and prostaglandin F2α-treated rats, while the other compounds had no effect. We also studied the effect of adrenergic antagonists on the release of prolactin and lactogenesis induced by the physiological decrease in progesterone at the end of pregnancy. On day 21 of pregnancy at 18.00 h, serum progesterone levels in intact rats were lower than 40 nmol/l, while serum prolactin and casein and lactose concentrations in the mammary gland were higher compared with values measured at 12.00 h on day 20. Treatments with propranolol, metoprolol or prazosin administered at 20.00 h on day 20 and 08.00 and 14.00 h on day 21 of pregnancy were capable of significantly reducing serum prolactin concentrations while only propranolol decreased mammary casein and lactose. The effect of propranolol was not mediated through a reduction in serum placental lactogen measured by Nb2 lymphoma cell bioassay. These results show that the adrenergic system participates, through α1 and β1 receptors, in the regulation of prolactin release induced by the decrease in progesterone in pregnant rats. They also show that β2-adrenergic receptors play a role in the induction of casein and lactose synthesis in the mammary gland. Journal of Endocrinology (1991) 129, 343–350


1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.


2013 ◽  
Vol 100 (3) ◽  
pp. S7 ◽  
Author(s):  
M. Li ◽  
Y. Xie ◽  
H. Park ◽  
A. Kumar ◽  
G. Hubert ◽  
...  

1958 ◽  
Vol 16 (3) ◽  
pp. 237-260 ◽  
Author(s):  
B. A. CROSS

SUMMARY The spontaneous motility of the intact uterus of spayed oestrogenized rabbits under sodium pentobarbitone anaesthesia has been recorded. Both uteri of each animal behaved similarly, and contractions often appeared to be synchronous. Small changes of load affected the amplitude of contractions, but did not alter uterine responsiveness to neurohypophysial or adrenomedullary hormones. Mid-thoracic section of the spinal cord obliterated spontaneous motility of the uterus; spinal anaesthesia did not. Spontaneous motility persisted for as long as 7 hr after decerebration and removal of the pituitary gland. The threshold dose of oxytocin for activating the oestrogenized uterus was the same as that for the lactating mammary gland, i.e. 1–5 mu. Doses up to 50 mu. usually gave an increase in frequency and amplitude of contractions. In the same dose range vasopressin either had little effect or inhibited spontaneous uterine motility, although milk ejection was stimulated. Slow infusion of oxytocin at rates of 1·5–48 mu./min produced graded increases in the rate and depth of uterine contractions and, at the same time, in similarly treated, lactating animals, rhythmic milk-ejection responses which at the higher rates of infusion merged to give a tetanic (plateau) type of milk ejection. Adrenaline or noradrenaline in doses of 1–5 μg produced diphasic uterine responses, initial contractions being followed by inhibition of spontaneous motility. They also inhibited the uterine, as well as the milk-ejection response to oxytocin injected 10–30 sec later. The inhibitory effect of adrenaline on both organs was about twice that of noradrenaline. The above-mentioned responses to adrenaline and oxytocin could also be elicited by electrical stimulation of the hypothalamus. Stimuli in the dorsal, lateral, perifornical and posterior hypothalamic areas produced effects equivalent to those of 1–5 μg adrenaline on both the uterus and mammary gland. These responses were abolished by mid-thoracic section of the spinal cord or by spinal anaesthesia. In such preparations responses typical of those produced by oxytocin were seen in both organs after stimulation of the paraventricular nuclei, supraoptic nuclei and the hypothalamo-hypophysial nerve pathways of the tuber cinereum and neural stalk. Dilatation of the vagina (or rectum) gave rise to a uterine response similar to that resulting from adrenaline or noradrenaline. The response was abolished by spinal anaesthesia, but not by mid-thoracic spinal section or decerebration. The same stimuli also produced 'bearing down' contractions of the abdominal muscles. Contractions of the uterus could also be elicited by mechanical stimuli, in the absence of functional spinal connexions.


1984 ◽  
Vol 52 (1) ◽  
pp. 131-137 ◽  
Author(s):  
G. R. Herzberg ◽  
Minda Rogerson

1. The effect of feeding casein, lactalbumin, soya-bean protein, gluten or gelatin on hepatic lipogenesis and the levels of hepatic fatty acid synthetase (FAS), glucose-6-phosphate dehydrogenase (EC 1. 1. 1.49; G6PD), malic enzyme (EC 1. 1. 1.40; ME) ATP-citrate lyase (EC 4. 1. 3. 8; CL), acetyl CoA carboxylase (EC 6.4.1.2; ACCx) and glucokinase (EC 2. 7. 1. 2; GK) was examined in young growing rats.2. The total activities of ACCx, FAS, CL, GK, G6PD, GK, ME and fatty acid synthesis in vivo were positively correlated with protein quality.3. The specific activities of ACCx, FAS, CL, G6PD and fatty acid synthesis in vivo were positively correlated with protein quality.4. The specific activities of GK and ME were unrelated to protein quality.5. The results demonstrate a dissociation between ME and hepatic lipogenesis and suggest a role for the NADPH generated by ME which is not related to the needs of fatty acid synthesis.


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