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High‐refined carbohydrate diet leads to polycystic ovary syndrome-like features and reduced ovarian reserve in female rats
Toxicology Letters ( IF 2.9 ) Pub Date : 2020-10-01 , DOI: 10.1016/j.toxlet.2020.07.002
Oscar M S Niño 1 , Charles S da Costa 2 , Karine M Torres 2 , Jordana F Zanol 2 , Leandro C Freitas-Lima 2 , Leandro Miranda-Alves 3 , Jones B Graceli 2
Affiliation  

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.

中文翻译:

高精制碳水化合物饮食导致雌性大鼠多囊卵巢综合征样特征和卵巢储备减少

肥胖与多种女性生殖并发症有关,例如多囊卵巢综合征 (PCOS)。这种关系的确切机制尚不清楚。以前很少有研究使用含有精制碳水化合物 (HCD) 的饮食导致肥胖,目前尚不清楚 HCD 是否与生殖功能障碍有关。在这项调查中,我们评估了亚慢性 HCD 暴露是否会导致生殖和其他异常。雌性大鼠喂食 HCD 15 天,并评估代谢结果和生殖道形态生理学。我们进一步评估了生殖道炎症、氧化应激 (OS) 和纤维化。HCD 大鼠表现出代谢障碍,例如体重/肥胖增加、脂肪细胞肥大、血脂异常、葡萄糖耐量和胰岛素抵抗 (IR) 和高瘦素血症。观察到 HCD 生殖道功能不正常。具体而言,观察到不规则的发情周期、高 LH 水平和异常的卵巢形态以及原始和初级卵泡数量的减少,表明卵巢储备枯竭。不正常的卵泡发育和窦卵泡、黄体和颗粒层面积的减少以及囊性卵泡的增加是明显的。在 HCD 大鼠中观察到子宫萎缩和子宫内膜腺 (GE) 数量减少。在 HCD 大鼠中观察到生殖道炎症、OS 和纤维化。此外,在体重/肥胖和 IR 与发情周期长度、囊性卵泡、卵巢储备、GE 和其他异常之间观察到强烈的正相关。因此,
更新日期:2020-10-01
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