Granholm N H, Jeppesen K W, Japs R A
J Reprod Fertil. 1986 Jan;76(1):279-87. doi: 10.1530/jrf.0.0760279.
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.
120日龄及以上的肥胖Ay/a雌性小鼠，与年龄匹配的a/a对照（C57BL/6J品系）相比，表现出异常的发情周期，其特征为真正发情期涂片频率降低、与经证实的a/a雄性小鼠的交配成功率下降、子宫重量降低以及排卵率降低。外源性促性腺激素（孕马血清促性腺激素/人绒毛膜促性腺激素）使肥胖Ay/a雌性小鼠的排卵部分恢复到接近对照水平，这表明Ay/a卵巢组织对促卵泡生成素和促黄体生成素敏感，至少在超排卵水平上是如此。因此，肥胖Ay/a雌性小鼠体内内源性促性腺激素的浓度和/或卵巢靶细胞对促性腺激素的敏感性可能受损。异常的交配行为、子宫重量降低和受孕率降低强烈提示卵巢类固醇缺乏，这可能是内源性促性腺激素活性降低的继发效应。与其他肥胖啮齿动物综合征（如ob/ob、db/db和fa/fa）一样，一种可能的由Ay引起的下丘脑基本病变与我们的数据一致。
