Leptin Promotes the Development of Mouse Preimplantation Embryos in Vitro

Kawamura, Kazuhiro; Sato, Naoki; Kodama, Hiroyuki; Fukuda, Jun; Tanikawa, Hideo; Honda, Yoshiyuki; Tanaka, Toshinobu

doi:10.1210/en.143.5.1922

Cited by 67 publications

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“…In the ovary, leptin receptor mRNA and protein are expressed in granulosa, theca, luteal, and microvascular endothelial cells [4][5][6][7], as well as oocytes [7,8]. Leptin receptors are also present in early cleavagestage embryos and blastocysts [9]. That leptin is obligatory for reproduction is demonstrated by the complete infertility of the leptin-deficient (ob/ob) mouse, which is reversible by exogenous leptin administration [10].…”

Section: Introductionmentioning

confidence: 99%

Declining fertility in the lethal yellow mouse is related to progressive hyperleptinemia and leptin resistance

2005

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-Mice possessing the lethal yellow mutation (C57BL/6J A y /a) become obese and develop hyperleptinemia and leptin resistance as they age. To determine the relationship between altered leptin physiology and reproductive function in these mice, we compared body weight (BW), serum leptin concentration, ovulation rate, and in vitro blastocyst development among 120-and 180-d-old lethal yellow and black non-mutant (a/a) mice. Estrous female yellow and black mice were mated with fertile black males. Oviducts were flushed ~ 36 h after mating and the recovered embryos were cultured for 96 h. BW, serum leptin levels, and the leptin:BW ratio differed among groups as follows: 180-d yellow > 120-d yellow > 180-d black = 120-d black. Ovulation rate was similar among 120-d yellow and black, and 180-d black mice. Among 180-d yellow mice, five of twelve mice failed to ovulate, but the other seven mice ovulated a similar number of oocytes as their black counterparts (8.4 ± 0.9 versus 8.0 ± 1.3). Non-ovulators had higher (P < 0.05) leptin levels (56.6 ± 1.8 ng·mL -1 ) than ovulators (46.2 ± 3.5), but BW did not differ significantly. Fewer embryos from 180-d yellow mice reached the blastocyst stage in culture than did the embryos from black mice (55% versus 83%, P < 0.05). Moreover, blastocyst development in 180-d old yellow mice negatively correlated with leptin levels (r = -0.797, P = 0.032) and leptin:BW ratio (r = -0.847, P = 0.016), but not with BW. Declining reproductive function in lethal yellow mice appears to be related to increasing levels of leptin and progression of leptin resistance. obesity / leptin / agouti / reproduction

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Section: Introductionmentioning

confidence: 99%

Declining fertility in the lethal yellow mouse is related to progressive hyperleptinemia and leptin resistance

2005

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“…For example, pig EGA takes place at the four-cell stage and studies by Craig et al (2005) detected the LEPR gene transcript from the four-cell pig embryos onwards. In the mouse, major EGA occurs at the two-cell stage and according to Kawamura et al (2002) LEPR gene mRNA was observed in two blastomere embryos, morulae and blastocysts. In human development LEPR gene transcript was identified in oocytes and at all preimplantation stages (Cervero et al, 2004); however, this study only reported a qualitative aspect of gene expression and thus the information on the possible drop in the mRNA level at the time of EGA was not available.…”

Section: Discussionmentioning

confidence: 99%

“…LEP mRNA was detected in mouse blastocysts and the mRNA for two long leptin receptor isoforms (Ob-Ra and OB-Rb) was identified in mouse oocytes, zygotes, twocell embryos, morulae and blastocysts (Kawamura et al, 2002). The LEPR gene transcript has not been observed in four-and eight-cell mouse embryos (Kawamura et al, 2002). Human embryos express LEPR at all preimplantation stages (Cervero et al, 2004) whereas it is expressed in pig embryos from the four-cell stage onwards (Craig et al, 2005).…”

Section: Introductionmentioning

confidence: 98%

“…Leptin may have diverse regulatory actions with involvement in the preimplantation period of embryonic development as well as implantation (trophoblast invasion) and foetal growth (Fedorcsak and Storeng, 2003;Swain et al, 2004;Craig et al, 2005;Yoon et al, 2005;Yang et al, 2006). Transcripts for the leptin gene (LEP) and the leptin receptor gene (LEPR) were identified in several tissues or cell types related to reproduction (ovaries, testis, placenta, endometrium, granulosa and cumulus oophorus cells) (Cioffi et al, 1997) as well as human and mouse oocytes and preimplantation embryos Kawamura et al, 2002;Kawamura et al, 2003). LEP mRNA was detected in mouse blastocysts and the mRNA for two long leptin receptor isoforms (Ob-Ra and OB-Rb) was identified in mouse oocytes, zygotes, twocell embryos, morulae and blastocysts (Kawamura et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Transcripts for the leptin gene (LEP) and the leptin receptor gene (LEPR) were identified in several tissues or cell types related to reproduction (ovaries, testis, placenta, endometrium, granulosa and cumulus oophorus cells) (Cioffi et al, 1997) as well as human and mouse oocytes and preimplantation embryos Kawamura et al, 2002;Kawamura et al, 2003). LEP mRNA was detected in mouse blastocysts and the mRNA for two long leptin receptor isoforms (Ob-Ra and OB-Rb) was identified in mouse oocytes, zygotes, twocell embryos, morulae and blastocysts (Kawamura et al, 2002). The LEPR gene transcript has not been observed in four-and eight-cell mouse embryos (Kawamura et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Gene expression and protein distribution of leptin and its receptor in bovine oocytes and preattachment embryos produced in vitro

Madeja

Warzych

Peippo

et al. 2009

Animal

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Many investigations point out the important role of leptin during the preimplantation development. Transcripts for the leptin gene (LEP) and its receptor (LEPR) have been identified in several tissues related to reproduction (e.g. ovaries, testis and oviduct) in both human and mouse. This work shows for the first time the expression and distribution patterns of LEP and LEPR in bovine oocytes and in vitro-produced embryos. Gene expression was analysed by reverse transcription PCR and real-time PCR, and the proteins were localised by immunostaining. This study included immature and mature oocytes, zygotes, two-, four-, eight-to 16-cell embryos, morulae and blastocysts and the LEP transcript was identified throughout all stages of bovine preimplantation development. However, mRNA for the LEPR gene was detected at all stages, excluding four-cell embryos. Expression of both LEP and LEPR genes was reduced at the eight-to 16-cell stage. This in addition to the absence of LEPR mRNA in four-blastomere embryos may suggest that maternally derived transcripts degenerate towards the eight-to 16-cell stage coinciding with embryonic genome activation at eight-to 16-cell stage and subsequent appearance of embryonic mRNA. Immunofluorescent staining demonstrated that LEP and LEPR proteins form a spherical rim beneath the oolemma. After maturation, however, the proteins became evenly distributed within the cytoplasm. In two-to eight-cell embryos, fluorescence was observed in the apical surface of the blastomeres, and from 10-to 16-cell stage in the apical region of outer blastomeres. This pattern persisted to the blastocyst stage, leading to LEP and LEPR distribution within trophoblast cells, but not in the inner cell mass. These results support previous findings on polar distribution of proteins within mammalian oocytes and embryos, as well as suggests leptin's potential role during early mammalian development and implantation.

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Management of reproduction and pregnancy complications in maternal obesity: Which role for dietary polyphenols?

et al. 2013

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Obesity is a global and dramatic public health problem; maternal obesity represents one of the main risk factors of infertility and pregnancy complications as it is associated with adverse maternal and offspring outcomes. In the last few years, adipose tissue dysfunction associated with altered adipocytokine secretion has been suggested to play a critical role in all the phases of reproductive process. Obesity is a nutrition-related disorder. In this regard, dietary intervention strategies, such as high intake of fruit and vegetables, have shown significant effects in both preserving health and counteracting obesity-associated diseases. Evidence has been provided that polyphenols, important constituents of plant-derived food, can influence developmental program of oocyte and embryo, as well as pregnancy progression by modulating several cellular pathways. This review will examine the controversial results so far obtained on adipocytokine involvement in fertility impairment and pregnancy complications. Furthermore, the different effects exerted by polyphenols on oocyte, embryo, and pregnancy development will be also taken in account.

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Leptin Promotes the Development of Mouse Preimplantation Embryos in Vitro

Cited by 67 publications

References 0 publications

Declining fertility in the lethal yellow mouse is related to progressive hyperleptinemia and leptin resistance

Declining fertility in the lethal yellow mouse is related to progressive hyperleptinemia and leptin resistance

Gene expression and protein distribution of leptin and its receptor in bovine oocytes and preattachment embryos produced in vitro

Management of reproduction and pregnancy complications in maternal obesity: Which role for dietary polyphenols?

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