Caloric restriction promotes the reserve of follicle pool in adult female rats by inhibiting the activation of mammalian target of rapamycin signaling

• Published in: Reproductive sciences (Thousand Oaks, Calif.) Vol. 22; no. 1; p. 60
• Main Authors: Li, Li, Fu, Yu-cai, Xu, Jin-jie, Lin, Xuan-hao, Chen, Xiao-chun, Zhang, Xing-mei, Luo, Li-li
• Format: Journal Article
• Language: English
• Published: United States 01-01-2015
• Subjects: Animal Nutritional Physiological Phenomena; Animals; Body Weight; Caloric Restriction; Cell Proliferation; Diet, High-Fat; Estrogens - blood; Female; Follicle Stimulating Hormone - blood; Luteinizing Hormone - blood; Nutritional Status; Ovarian Follicle - enzymology; Phosphorylation; Rats, Sprague-Dawley; Ribosomal Protein S6 Kinases, 70-kDa - metabolism; Signal Transduction; Time Factors; TOR Serine-Threonine Kinases - metabolism; mTOR; estrogen; caloric restriction; luteinizing hormone; primordial follicle
• ISSN: 1933-7205
• DOI: 10.1177/1933719114542016

Caloric restriction (CR) is known to increase the number of primordial follicles and prolong the reproductive life span. However, how CR modulates follicular development is not well understood. In the present study, we examined the effects of CR on follicular development in rats and investigated the underlying mechanism. After 10 weeks of CR or high-fat diet, ovarian follicles at different developmental stages were examined by histological analysis. Plasma levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estrogen (ESG) were measured, and the levels of mammalian target of rapamycin (mTOR), p70S6 kinase (p70S6K), and phosphorylated p70S6K in the ovary were detected by Western blot. The results showed that the reserve of follicle pool in CR rats was increased, accompanied by decreased level of phosphorylated p70S6K in the ovary, and decreased serum LH, FSH, and ESG levels. Taken together, these results suggest that CR may suppress ovarian follicular development and enhance the follicle pool reserve by inhibiting mTOR signaling.