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Reproduction, Fertility and Development Reproduction, Fertility and Development Society
Vertebrate reproductive science and technology
RESEARCH ARTICLE

Low-density lipoprotein receptor affects the fertility of female mice

Tao Guo A B , Liang Zhang B , Dong Cheng C , Tao Liu A B , Liguo An B , Wei-Ping Li A D and Cong Zhang A B D
+ Author Affiliations
- Author Affiliations

A Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Center for Reproductive Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200135, China.

B Key Laboratory of Animal Resistance Research, College of Life Science, Shandong Normal University, 88 East Wenhua Road, Ji’nan, Shandong, 250014, China.

C Shandong Center for Disease Control and Prevention, 16992 Jingshi Road, Ji’nan, Shandong, 250014, China.

D Corresponding authors. Email: zhangxinyunlife@163.com; liweiping@renji.com

Reproduction, Fertility and Development 27(8) 1222-1232 https://doi.org/10.1071/RD13436
Submitted: 21 December 2013  Accepted: 7 May 2014   Published: 15 July 2014

Abstract

Low-density lipoprotein receptor (LDLR) has been demonstrated to play a central role in lipoprotein metabolism, with Ldlr-deficient (Ldlr–/–) mice developing severe dyslipidemia. In the present study we investigated whether Ldlr knockout could harm female reproduction and explored the mechanisms involved. The results indicate that although the number of litters born to Ldlr–/– mice did not differ significantly from that born to controls, the number of pups per litter was significantly lower in the former group. Interestingly, although Ldlr–/– mice were obese, the weight of their ovaries was lower than that in control mice. Serum cholesterol levels was significantly higher in Ldlr–/– mice than in their wild-type counterparts. In contrast, there were significant decreases in cholesterol, triglyceride and total lipid levels in ovaries of Ldlr–/– mice. Both ovarian lipid deposition, as detected by Oil red O staining, and lipid droplets, as evaluated by transmission electron microscopy, supported decreased lipid levels in ovaries from Ldlr–/– mice. In addition, Ldlr–/– mice had fewer ovarian follicles, more atretic follicles, lower oestrogen levels and spent significantly less time in oestrus than did the controls. Superovulation assays indicated immature Ldlr–/– mice ovulated fewer ova than controls. These results indicate that lack of Ldlr results in dyslipidaemia and poor fertility.

Additional keywords: atresia, dyslipidaemia, Ldlr, oestrogen.


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