High‐refined carbohydrate diet leads to polycystic ovary syndrome-like features and reduced ovarian reserve in female rats. (10th October 2020)

• Record Type: Journal Article
• Authors: Niño, Oscar M.S.; da Costa, Charles S.; Torres, Karine M.; Zanol, Jordana F.; Freitas-Lima, Leandro C.; Miranda-Alves, Leandro; Graceli, Jones B.
• Is Part Of: Toxicology letters. Volume 332(2020)
• Page Start: 42
• Page End: 55
• Publication Date: 2020-10-10
• Subjects: High-refined carbohydrate diet -- Obesity -- Leptin -- Polycystic ovary syndrome -- Ovarian reserve -- Reproductive toxicology; Toxicology -- Periodicals; 363.179
• DOI: 10.1016/j.toxlet.2020.07.002
• Languages: English
• ISSNs: 0378-4274

Abstract

Graphical abstract: Highlights: High carbohydrate diet is a diet-induced obese model. High carbohydrate diet induces polycystic ovary syndrome features. High carbohydrate diet impairs ovarian follicular reserve. High carbohydrate diet induces reproductive tract inflammation and oxidative stress. High carbohydrate diet induces reproductive tract fibrosis. Abstract: Obesity is associated with several female reproductive complications, such as polycystic ovary syndrome (PCOS). The exact mechanism of this relationship remains unclear. Few previous studies using diet containing refined carbohydrate (HCD) leading to obesity have been performed and it is unclear if HCD is linked with reproductive dysfunctions. In this investigation, we assessed whether subchronic HCD exposure results in reproductive and other irregularities. Female rats were fed with HCD for 15 days and metabolic outcomes and reproductive tract morphophysiology were assessed. We further assessed reproductive tract inflammation, oxidative stress (OS) and fibrosis. HCD rats displayed metabolic impairments, such as an increase in body weight/adiposity, adipocyte hypertrophic, abnormal lipid profile, glucose tolerance and insulin resistance (IR) and hyperleptinemia. Improper functioning of the HCD reproductive tract was observed. Specifically, irregular estrous cyclicity, high LH levels and abnormal ovarian morphology coupled with reduction in primordial and primary follicle numbers was observed, suggesting ovarian reserve depletion. Improper follicular development and a reduction in antral follicles, corpora lutea and granulosa layer area together with an increase in cystic follicles were apparent. Uterine atrophy and reduction in endometrial gland (GE) number was observed in HCD rats. Reproductive tract inflammation, OS and fibrosis were seen in HCD rats. Further, strong positive correlations were observed between body weight/adiposity and IR with estrous cycle length, cystic follicles, ovarian reserve, GE and other abnormalities. Thus, these data suggest that the subchronic HCD exposure led to PCOS-like features, impaired ovarian reserve, GE number, and other reproductive abnormalities in female rats.