Caloric restriction promotes the reproductive capacity of female rats via modulating the level of insulin-like growth factor-1 (IGF-1).

Gen Comp Endocrinol

Department of Gynaecology and Obstetrics of the First Affiliated Hospital, Medical College, Shantou University, Shantou 515041, China.

Published: November 2011

AI Article Synopsis

  • The study investigates how caloric restriction (CR) affects the reproductive lifespan in rats and the role of insulin-like growth factor-1 (IGF-1) in this process.
  • Results show that CR lowers IGF-1 levels, leading to decreases in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estrogen (ESG) levels, while promoting the survival of primordial and surviving follicles.
  • Immunohistochemical analysis reveals that IGF-1 is mainly found in the cytoplasm of healthy granulosa cells but absent in deteriorating follicles, indicating that CR may enhance female reproductive capacity by regulating IGF-1 levels and subsequent hormone release.

Article Abstract

The insulin-like growth factor-1 (IGF-1) plays an important role in the regulation of reproductive function. In the present study, we examined the effects of caloric restriction (CR) on the reproductive lifespan in rats and investigated the potential role of IGF-1. After 10 weeks of treatment, we determined the distribution of the ovarian follicles at various stages and measured the plasma level of IGF-1, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estrogen (ESG). Our results show that IGF-1 level was decreased after CR and correlated with the decrease in the levels of LH, FSH and ESG. Moreover, a higher percentage of primordial follicles and surviving follicles was observed in CR rats than in control rats (P<0.05). Immunohistochemical analysis showed that IGF-1 was extensively expressed in the cytoplasm of granulosa cells in the surviving follicles at different stages but not in the atretic follicles. Taken together, these results suggest that caloric restriction promotes the reproductive capacity of female rats via modulating the level of IGF-1, which then regulate pituitary gonadotrope cells to reduce the release of LH, FSH and ESG, and modulate follicular development.

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Source
http://dx.doi.org/10.1016/j.ygcen.2011.09.005DOI Listing

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