Regulation of Gonadotrophin Secretion in the Prepubertal Period

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Abstract
The plerocercoid larvae of the tapeworm, Spirometra mansonoides, produce a growth factor, called plerocercoid growth factor (PGF) that suppresses endogenous growth hormone (GH). Treatment (infection) with 10 plerocercoids at weaning age (22 days of age) delayed puberty onset in the female rat. First ovulation was at 34.0 ± 0.6 days in controls and at 38.6 ± 0.9 days in worm-treated rats (p < 0.01). When basal serum hormone levels were measured at 08.00–09.00 h at several times during the prepubertal period, no changes were found in FSH, LH or prolactin. Growth hormone (GH) was below measurable levels in both groups before day 27. GH of infected rats remained significantly suppressed at least until the second metestrus. Thyroxine (T4) was significantly lower in worm-treated animals beginning at 26 days of age and remained depressed until 33 days of age. Gonadotrophin regulation was assessed by measuring the rate of rise of serum FSH and LH during the first 48 h after castration at 25, 28 and 32 days of age and on the day of the second metestrus. The rate of increase in FSH fell with age in both groups but was significantly less at all prepubertal ages in worm-treated rats. The LH response was less in castrated postpubertal controls but there was not a clear-cut progressive fall with age. The LH response was less in worm-treated rats at all the prepubertal ages tested but not at second metestrus. To determine whether the lack of difference between the two metestrus groups was due to a diminution of the worm effect, worms were implanted at 30 days of age and the castration response at second metestrus was compared to that obtained in rats given worms at 22 days of age. The FSH and LH responses in both sets of worm-treated rats were comparable, indicating that the loss of suppression relates to age rather than a decreased secretion of PGF. To determine whether the acute suppression of the castration response would persist, measurements of serum FSH and LH were made 4, 7 and 14 days after castration at 25 days of age. By 4 days after castration, FSH and LH were comparable in the two groups. This occurred despite the continuation of T4 and GH deficiency at that age. When the castration response was suppressed by the daily administration of 0.05 or 0.5 μg estradiol benzoate (EB), worm-treated animals showed a greater sensitivity to both doses of EB. Delay in puberty onset in worm-treated animals is associated with both T4 and GH deficiency but the suppression of the response of FSH and LH to castration and the heightened sensitivity to estrogen are not attributable solely to these deficits.