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

Oleh:

Zhang, Yuehui ; Hu, Min ; Ma, Hongxia ; Qu, Junwei

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 97 no. 05 (May 2012), page 1183-1191.
Topik: REPRODUCTIVE BIOLOGY; Db/db mice; leptin receptor; reproduction; ovary; leptin signaling; PCOS

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2012.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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

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