Insulin receptor and IGF1R are not required for oocyte growth, differentiation, and maturation in mice

J. L. Pitetti, D. Torre, B. Conne, M. D. Papaioannou, C. R. Cederroth, S. Xuan, R. Kahn, L. F. Parada, J. D. Vassalli, A. Efstratiadis, S. Nef

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

In mammals, insulin and insulin-like growth factors (IGFs: IGF1 and IGF2) act through 2 structurally related receptors, the insulin receptor (INSR) and the type 1 IGF receptor (IGF1R), both of which are expressed in developing oocytes. IGF1 plays an important role in female reproduction, and female Igf1 knockout mice fail to ovulate and are infertile. On the other hand, little is known about the in vivo role of the insulin signaling pathway in oocytes during follicular development, although exposure to insulin or IGF1 in vitro improves oocyte maturation. To further address the significance of insulin/IGF signaling, we used conditional mutant mice and ablated the function of the genes encoding INSR, IGF1R, or both receptors specifically in developing mouse oocytes. Our genetic evidence showed unexpectedly that the female reproductive functions are not affected when Insr, Igf1r or both Insr;Igf1r are ablated in oocytes, as the female mice are fertile and exhibit normal estrous cyclicity, oocyte development and maturation, parturition frequency, and litter size. In view of these novel observations indicating that the insulin/IGF signaling is not essential in oocytes, the IGF1-dependent female fertility is re-evaluated and discussed.

Original languageEnglish (US)
Pages (from-to)264-272
Number of pages9
JournalSexual Development
Volume3
Issue number5
DOIs
StatePublished - Dec 2009

Fingerprint

Insulin Receptor
Oocytes
Insulin
Growth
In Vitro Oocyte Maturation Techniques
Litter Size
IGF Type 1 Receptor
Somatomedins
Periodicity
Knockout Mice
Reproduction
Fertility
Mammals
Parturition
Genes

Keywords

  • Differentiation
  • Fertility
  • Growth
  • Igf1r
  • Insr Maturation
  • Mouse
  • Oozyte

ASJC Scopus subject areas

  • Developmental Biology
  • Embryology
  • Endocrinology, Diabetes and Metabolism

Cite this

Pitetti, J. L., Torre, D., Conne, B., Papaioannou, M. D., Cederroth, C. R., Xuan, S., ... Nef, S. (2009). Insulin receptor and IGF1R are not required for oocyte growth, differentiation, and maturation in mice. Sexual Development, 3(5), 264-272. https://doi.org/10.1159/000252813

Insulin receptor and IGF1R are not required for oocyte growth, differentiation, and maturation in mice. / Pitetti, J. L.; Torre, D.; Conne, B.; Papaioannou, M. D.; Cederroth, C. R.; Xuan, S.; Kahn, R.; Parada, L. F.; Vassalli, J. D.; Efstratiadis, A.; Nef, S.

In: Sexual Development, Vol. 3, No. 5, 12.2009, p. 264-272.

Research output: Contribution to journalArticle

Pitetti, JL, Torre, D, Conne, B, Papaioannou, MD, Cederroth, CR, Xuan, S, Kahn, R, Parada, LF, Vassalli, JD, Efstratiadis, A & Nef, S 2009, 'Insulin receptor and IGF1R are not required for oocyte growth, differentiation, and maturation in mice', Sexual Development, vol. 3, no. 5, pp. 264-272. https://doi.org/10.1159/000252813
Pitetti, J. L. ; Torre, D. ; Conne, B. ; Papaioannou, M. D. ; Cederroth, C. R. ; Xuan, S. ; Kahn, R. ; Parada, L. F. ; Vassalli, J. D. ; Efstratiadis, A. ; Nef, S. / Insulin receptor and IGF1R are not required for oocyte growth, differentiation, and maturation in mice. In: Sexual Development. 2009 ; Vol. 3, No. 5. pp. 264-272.
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