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父母肥胖症以不同的方式重塑 F1 代雌性大鼠的卵巢线粒体生物发生。

Maternal and paternal obesity differentially reprogram the ovarian mitochondrial biogenesis of F1 female rats.

机构信息

Department of Biochemistry, Medical Research Institute, Alexandria University, 165 El-Horreya Avenue, EL-Hadara, POB: 21561, Alexandria, Egypt.

Department of Pathology, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt.

出版信息

Sci Rep. 2023 Sep 19;13(1):15480. doi: 10.1038/s41598-023-42468-5.

Abstract

Obesity has harmful consequences on reproductive outcomes and the rapid increase in obesity is assumed to be influenced by epigenetics and trans-generation effects. Our study aimed to explore the effect of maternal and/or paternal obesity on the ovarian tissues of the first-generation female offspring in rats. The study was conducted on 40 adult Wistar albino rats (20 males and 20 females). Obesity was induced by feeding them an obesogenic diet for 3 months. The pregnancy was induced in the females by mating with males in four combinations: healthy mother with healthy father (control parents, CP), healthy mother with obese fathers (OF), obese mothers with healthy father (OM), and obese mother with obese father (obese parents, OP). After delivery, the female offspring at two months were sacrificed, and the blood and ovarian tissues were collected to assess the studied parameters. Our result showed differential impacts of maternal and paternal obesity on the ovarian health of the female offspring. The female offspring of obese OM or OP showed early signs of obesity. These metabolic abnormalities were associated with signs of ovarian lesions, impaired folliculogenesis, and decreased oocyte quality and also showed significant alterations in mitochondrial biogenesis, redox status, inflammation, and microRNAs expression (miR-149 and miR-494). In conclusion, altered ovarian expression of microRNAs and associated impaired mitochondrial biogenesis pathways may be the root causes for the observed intergeneration transmission of the obesogenic phenotype.

摘要

肥胖对生殖结果有不良影响,而肥胖的快速增加被认为受到表观遗传学和跨代效应的影响。我们的研究旨在探讨母系和/或父系肥胖对第一代雌性大鼠卵巢组织的影响。该研究在 40 只成年 Wistar 白化大鼠(20 只雄性和 20 只雌性)中进行。通过喂食致肥胖饮食 3 个月来诱导肥胖。通过将雌性与雄性交配,在四种组合中诱导怀孕:健康母亲与健康父亲(对照父母,CP)、健康母亲与肥胖父亲(OF)、肥胖母亲与健康父亲(OM)和肥胖母亲与肥胖父亲(肥胖父母,OP)。分娩后,将两个月大的雌性后代处死,采集血液和卵巢组织以评估研究参数。我们的结果显示母系和父系肥胖对雌性后代的卵巢健康有不同的影响。肥胖 OM 或 OP 的雌性后代出现肥胖的早期迹象。这些代谢异常与卵巢损伤、卵泡发生受损、卵母细胞质量下降以及线粒体生物发生、氧化还原状态、炎症和 microRNAs 表达(miR-149 和 miR-494)的显著改变有关。总之,microRNAs 的卵巢表达改变和相关的受损线粒体生物发生途径可能是观察到肥胖表型的跨代传递的根本原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad2a/10509203/985a52aa1351/41598_2023_42468_Fig1_HTML.jpg

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