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T. J. McCLURE

Summary.

Daily treatment with progesterone and chorionic gonadotrophin was found to protect pregnancy in fasted mice so that it lasted at least 6 days longer than in control mice fasted from the end of the 3rd to 5th days after mating. Pregnancy could not, however, be maintained beyond the 14th or 15th day by these means. The pathogenesis of the embryonic mortality caused by fasting, therefore, appears to involve a failure of hypophyseal gonadotrophic function. Adrenalectomy and implantation with desoxycorticosterone acetate did not protect pregnancy in fasted rats, suggesting that the mortality was not caused by hypersecretion of corticosterone.

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T. J. McCLURE

Summary.

Experiments designed to find the pathogenesis of the infertility caused by fasting mice for 18 to 48 hr at about the time of mating showed that: (a) within 4 hr of removal of all food the blood-glucose level fell to about half, and that this fall was delayed for about 24 hr by adding glucose to the drinking water; (b) protamine zinc insulin reduced both blood-glucose level and littering rate; (c) 2-deoxy-d-glucose (2dg) inhibited ovulation and caused the death of tubal ova; (d) fasting, insulin and 2dg appeared to cause similar effects upon the fertility; and (e) the expected infertility of fasted mice was prevented by the administration of human chorionic gonadotrophin and progesterone at the appropriate times.

The evidence suggested that the primary biochemical disturbance was hypoglycaemia and that this inhibited adenohypophysial gonadotrophic function.

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T. J. McCLURE

Summary.

Fasting male mice for up to 30 hr did not affect their libido, but fasting for 36 or 48 hr did so for 2 days after the end of the fast. Fasting male mice for up to 48 hr did not affect their fertility on any of the succeeding days.

Fasting both male and female mice for up to 30 hr did not affect the number and distribution of females mated. Fasting for 36 or 48 hr reduced the number of females mated in both the first 2 days and the first 5 days after the end of fasting and altered the distribution of mating in the first 5 days much more than when only males were fasted. Fasting both males and females significantly reduced the littering rate of the females mated 0 to 2 days before or after the end of 18 to 48 hr fasting.

It is concluded that acute inanition in females for 18 to 30 hr at and about the time of mating can reduce fertility without markedly affecting the manifestation of oestrus and that a more prolonged period ofinanition of 36 hr or more also depresses oestrus. The essential factor in acute inanition appears to be an acute energy deficiency.

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T. J. McClure and J. Saunders

Summary. Food was withheld from female rats for 0–72 h at various stages of the oestrous cycle. Withholding food for periods of 24 h ending at 12:00 h on the day of pro-oestrus reduced the mating rate from 61 to 25% (P < 0·05) but not the pregnancy rate of those rats that mated. Fasting for 24 h ending at 18:00 h on the day of pro-oestrus reduced the pregnancy rate from 82 to 18% (P < 0·05) without affecting the mating rate and a 48-h fast starting at 12:00 h on the day of pro-oestrus reduced the pregnancy rate from 82 to 25% (P < 0·05). Withholding food for 23 h ending at 17:00 h on the day of pro-oestrus prevented the LH and prolactin surges normally present at 17:00 h on this day. The treatments had no apparent effect on the ability of the adenohypophysis to release LH in response to injections of GnRH. When ovariectomized female rats fasted for 0–72 h and given 2 injections of oestradiol dibenzoate to test the ability of the hypothalamus to respond to an increasing plasma oestradiol concentration by stimulating the release of LH, a fast for 24 h reduced and a fast for 72 h completely prevented LH release.