The impairment of reproduction in db/db mice is not mediated by intraovarian defective leptin signaling

We report on how impairment of reproduction in db mice is not mediated by intraovary intact/defective leptin signaling even in the face of a significantly divergent modulation by gonadotropins.

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Authors

Yuehui Zhang, M.D., Ph.D., Min Hu, M.D., Hongxia Ma, M.D., Ph.D., Junwei Qu, M.D., Ph.D., Yong Wang, Ph.D., Lihui Hou, M.D., Li Liu, M.D., Ph.D., Xiao-Ke Wu, M.D., Ph.D.

Vol 97, Issue 5, Pages 1183-1191

Abstract

Objective:

To demonstrate whether leptin modulates reproduction by a direct effect within the ovary.

Design:

Animal model.

Setting:

National Key Laboratory of Infertility.

Animal(s):

Adult female db/db mice.

Intervention(s):

Adult littermate wild-type (WT) and diabetic (db) leptin receptor (LR) mutant female mice were matched for the allograft of the ovary to construct new genotypic models, respectively. WT mouse received only one ovary from a WT or a db/db mouse (WT Ov-WT, WT Ov-db), and db/db mouse received one ovary from a WT or a db/db mouse (db Ov-WT, db Ov-db). WT and db/db mice received one ovary from a WT mouse and another ovary from a db/db mouse (WT Ov-WT/db, db Ov-WT/db) or received two ovaries all from a WT mouse (db Ov-WT/WT).

Main Outcome Measure(s):

Hormones, lipids, and reverse transcription polymerase chain reaction.

Result(s):

Both WT Ov-WT and WT Ov-db mice presented normal cycles, comparable serum E2 and FSH levels, and ovarian expressions of the Star, Cyp17, and Cyp19 mRNA, even with different ovary genotypes. In WT Ov-WT/db with hMG stimulation, db ovaries with LR mutation expressed higher Star, Cyp17, Cyp19, Jak2, Stat3, and Pias3 mRNA than in the basal state, whereas WT ovaries with intact LR expressed higher Star, Cyp17, and Cyp19 but divergently lower Jak2, Stat3, and Pias3 levels.

Conclusion(s):

We confirmed that impairment of reproduction in intact db/db mice is not mediated by intraovary intact/defective leptin signaling even in face of a divergent modulation by gonadotropins.

Read the full text at: http://www.fertstert.org/article/S0015-0282(12)00185-9/fulltext


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Fertility and Sterility

Editorial Office, American Society for Reproductive Medicine

Fertility and Sterility® is an international journal for obstetricians, gynecologists, reproductive endocrinologists, urologists, basic scientists and others who treat and investigate problems of infertility and human reproductive disorders. The journal publishes juried original scientific articles in clinical and laboratory research relevant to reproductive endocrinology, urology, andrology, physiology, immunology, genetics, contraception, and menopause. Fertility and Sterility® encourages and supports meaningful basic and clinical research, and facilitates and promotes excellence in professional education, in the field of reproductive medicine.

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