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N. H. Granholm and G. A. Dickens

Summary. This study was conducted to determine whether reproductive failures in ageing, obese lethal yellow (A y/a) females are due primarily to defects within A y/a ovaries or to systemic defects which may operate outside the ovaries. Reciprocal ovary transplantation between control (a/a) and lethal yellow (A y/a) females provided an experimental system to test the reproductive potential of not only A y/a ovaries in control (a/a) females but also control (a/a) ovaries in mutant (A y/a) females. Results on reproductive performance of all four combinations of grafts between A y/a and a/a mice proved that A y-induced reproductive failures are not due to intrinsic ovarian lesions but rather to defects operating extrinsically to the ovary. The hypothalamo–pituitary axis is a likely site for this reproductive lesion.

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N. H. Granholm, K. W. Jeppesen, and R. A. Japs

Summary. Obese Ay/a females of 120 days or older, when compared to age-matched a/a controls (strain C57BL/6J), exhibited abnormal oestrous cyclicity characterized by reduced frequencies of true oestrous-stage smears, decreased mating success to proven a/a males, lowered uterine weights, and depressed ovulation rates. Exogenous gonadotrophins (PMSG/hCG) partly restored ovulation in obese Ay/a females to near control levels, demonstrating the sensitivity of Ay/a ovarian tissues to FSH and LH, at least at superovulatory levels. Concentrations of endogenous gonadotrophins and/or sensitivity of ovarian target cells to gonadotrophins may therefore be impaired in obese Ay/a females. Aberrant copulatory behaviour, reduced uterine weights, and depressed conception rates strongly suggest ovarian steroid deficiencies, perhaps secondary effects of reduced endogenous gonadotrophin activity. As in other obese rodent syndromes (e.g. ob/ob, db/db, and fa/fa), a possible fundamental Ay-induced hypothalamic lesion is consistent with our data.