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The effects of IGF-I on bovine follicle development and IGFBP-2 expression are dose and stage dependent

Institute of Cell and Molecular Biology, Darwin Building, University of Edinburgh, King’s Buildings, Mayfield Road, Edinburgh EH9 3JR, UK, ¹ Division of Integrative Biology, Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, UK and ² School of Human Development, University of Nottingham, Queens Medical Centre, Nottingham NG7 2VH, UK

Correspondence should be addressed to E E Telfer; Email: Evelyn.Telfer{at}ed.ac.uk

This study aimed to determine the effect of insulin-like growth factor-I (IGF-I) on early antral bovine follicular development, and the expression of insulin-like growth factor-binding protein-2 (IGFBP-2). Antral follicles separated into three different size groups were cultured for 6 days in medium supplemented with either a low (10 ng/ml) or high (1 µg/ml) dose of human recombinant IGF-I. Oestradiol production by follicles in all size ranges, cultured in the presence of the high concentration of IGF-I, significantly increased by day 6 (P < 0.05). Follicles in the smallest size range, 165–215 µm, cultured in a high dose of IGF-I, were found to be significantly increased in size (P < 0.01). Oocyte health of the largest follicles (281–380 µm) was significantly improved by the addition of IGF-I to the culture medium. mRNA expression of IGFBP-2 was decreased in the granulosa cells of follicles, size range 216–280 µm, cultured with a high dose of IGF-I (P < 0.05). Granulosa cells (P < 0.05) and oocytes (P < 0.01) of the largest follicles (281–380 µm) showed a decrease in IGFBP-2 expression (protein) when cultured in the control and low-IGF-I treatment groups. Therefore, the response of a bovine follicle to IGF-I is both dose and stage dependent. This work supports a role for IGF-I in modulating somatic and germ-cell maturation and development in early antral follicles. Furthermore, the inverse relationship between the level of IGF-I stimulation and IGFBP-2 expression suggests a local regulatory system modulating IGF-I availability.

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