Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 245, Issue 1-2, Pages 121-127Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2005.11.003
Keywords
ovary; leptin deficiency; folliculogenesis; mouse
Categories
Funding
- NCRR NIH HHS [RR03024] Funding Source: Medline
- NICHD NIH HHS [HD41749, U54-HD28934] Funding Source: Medline
- NIGMS NIH HHS [GM08248] Funding Source: Medline
Ask authors/readers for more resources
Female leptin deficient (ob/ob) mice exhibit abnormal ovarian folliculogenesis resulting in an impaired ability to reproduce. This effect may be related to the hypogonadotropic state of these animals, or leptin may directly modulate ovarian follicle development. fit the present study we assessed whether exogenous gonadotropin administration would normalize folliculogenesis and induce ovulation in immature ob/ob animals. Eight 26-day-old ob/ob and eight control mice were injected sc with pregnant mare serum gonadotropin followed 48 It later with a sc injection of human chorionic gonadotropin. Animals were killed 24 h later. Gonadotropin (GTH) administration increased both ovarian and uterine weights in control mice, but this effect was attenuated in leptin deficient animals. The number of preantral follicles was greater in ob/ob mice than controls, but in GTH-treated animals the number of antral follicles was subnormal in the ovaries of leptin deficient animals. Ob/ob animals also failed to ovulate in response to GTH, and the protective actions of GTH against granulosa cell apoptosis and follicular atresia were attenuated in these animals. Interestingly, however, serum levels of estradiol and progesterone were higher in ob/ob mice than controls, regardless of whether or not the animals received GTH treatment. We conclude that the ovarian responsiveness to GTH is subnormal in leptin deficient animals suggesting that leptin may modulate the process of folliculogenesis by directly altering the sensitivity of the ovary to GTH. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available