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Z Lompo-Ouedraogo, D van der Heide, EM van der Beek, HJ Swarts, JA Mattheij and L Sawadogo

In view of the traditional belief that Acacia nilotica ssp adansonii (AN) can stimulate milk production in lactating women, experiments were performed to determine the effect of an aqueous extract of AN on milk production in rats. Female rats that received oral doses of aqueous extract of this plant during their first lactation produced about 59% more milk than controls (P<0.01). Pup weight gain was also significantly higher than that in the control group. A lower dose, comparable to that used by women to improve their milk yield, led to about 33% more milk with the same growth rate for pups as that in the high-dose group. The extract of AN was found to stimulate the synthesis and release of prolactin (PRL) significantly (P<0.05). In addition, the mammary glands of oestrogen-primed rats treated with the extract showed clear lobuloalveolar development with milk secretion. This study demonstrates that the aqueous extract of AN can stimulate milk production and PRL release in the female rat and could consequently have the properties claimed for lactating women.

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J A M Mattheij, J J M Swarts, P Lokerse, J T van Kampen and D Van der Heide

Abstract

The pituitary-ovarian axis was studied after withdrawal of thyroid hormone in 131I-radiothyroidectomized adult female rats. Oestrous cycles became prolonged and irregular within 2 weeks after the supply of thyroid hormone was stopped. If an LH surge occurred in hypothyroid rats on the day of vaginal pro-oestrus it was significantly greater in rats which had been made hypothyroid for 4–5 weeks than in controls; in hypothyroid rats with an LH surge on pro-oestrus, plasma progesterone showed a rise similar to that in controls at pro-oestrus; the ovulation rate was decreased in hypothyroid rats. About half of the rats from which blood was sampled daily in the afternoon between 7 and 18 days after tri-iodothyronine (T3) withdrawal had 1 day of pro-oestrus; on this day the LH surge was higher than in controls. On days 2 and 1 before and days 1 and 2 after this pro-oestrus, plasma progesterone was similar to that of controls on days 2 and 1 before and days 1 and 2 after pro-oestrus respectively. However, progesterone was higher in the period before and after these days. The other hypothyroid rats showed no pro-oestrus and no LH surge during this period, while their plasma progesterone levels were high on all days. On the morning of day 10 after T3 withdrawal and 5 days after the preceding pro-oestrus, most hypothyroid rats had high progesterone and low oestradiol plasma levels. In these rats, injection of gonadotrophin-releasing hormone caused a relatively small increase in LH; it did not stimulate the secretion of oestradiol or progesterone, and it did not induce ovulation. It was concluded that hypothyroidism induces major changes in the secretion of steroids by corpora lutea and growing follicles. Whether the changed steroid metabolism is the primary cause of the observed prolongation of the oestrous cycles, the increased pro-oestrous LH surge and the reduced ovulation rate remains to be investigated.

Journal of Endocrinology (1995) 146, 87–94

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P. H. L. M. Geelhoed-Duijvestijn, F. Roelfsema, J. P. Schröder-van der Elst, J. van Doorn and D. van der Heide

ABSTRACT

We have studied the effects of the administration of GH on plasma levels and peripheral production of tri-iodothyronine (T3) from thyroxine (T4) in thyroidectomized male Wistar rats given a continuous i.v. infusion of T4 (1 μg/100 g body weight per day) and GH (120 μg per day) for 3 weeks. Tracer doses of 131I-labelled T3 and 125I-labelled T4 were added to the infusion. At isotopic equilibrium (10 days after the addition of 125I-labelled T4) the rats were bled and perfused.

The plasma appearance rate for T3 was higher (10·6±1·3 vs 8·4 ± 2·8 pmol/h per 100 g body weight, P = 0·05) and plasma TSH was lower (246±24 vs 470±135 pmol/l, P<0·01) in GH-treated rats. The amount of T3 in liver (12·3 ±2·8 vs 5·5 ± 1·7 pmol/g wet weight, P<0·01), kidney (11·5±1·4 vs 6·5± 1·4 pmol/g wet weight, P <0·01) and pituitary (8·8 ±2·7 vs 4·8±0·5 pmol/g wet weight, P< 0·01) was higher than in controls, mainly as a result of an increased local production of T3 from T4, but plasma-derived T3 was also higher in most organs.

We found an increased intracellular T3 concentration in the pituitary which may be responsible for the lower plasma TSH concentration in the GH-treated rats. Since the increase in locally produced T3 is found particularly in liver, kidney and pituitary, typical organs that express 5′-deiodinase activity, we suggest that GH acts on thyroid hormone metabolism by stimulating type-I deiodinase activity.

Journal of Endocrinology (1992) 133, 45–49