Nutrition is an important source of exogenous AGEs and thermally processed foods present in western-style diets contain a large amount of these pro-inflammatory AGEs. Additionally, the intake of dietary AGEs could upregulate ovarian gene expression of inflammatory macrophage markers. The objective of this study was to investigate the effect of diet rich in AGEs on estrous cyclicity and ovarian function in a mouse model. Six-week old C57BL/6 J female mice were randomly subjected to either a diet low in AGEs (L-AGE) or a diet high in AGEs (H-AGE) for a total of 13 weeks. Experiments performed included daily vaginal smears to assess estrous cyclicity, ovarian superovulation with gonadotropins to assess the number of oocytes released, whole ovarian tissue mRNA quantification by RT-PCR to quantify genes involved in folliculogenesis, steroidogenesis, and macrophage markers, and ovarian morphology for follicle count. Outcome measures included estrous cyclicity, number of oocytes following superovulation, expression of genes involved in folliculogenesis, steroidogenesis, and macrophage infiltration as well as the number of primordial, primary, secondary, antral follicles and corpora lutea. Compared to mice on L-AGE diet, mice on H-AGE spent significantly longer time in the diestrus phase, had similar number of oocytes released following ovarian superovulation, and showed significant alterations in genes involved in steroidogenesis (increase in Star mRNA expression levels) and folliculogenesis (increase in Gdf-9 and Fshr mRNA expression levels). Mouse macrophage marker F4/80 mRNA expression was upregulated in mice on H-AGE diet compared to mice on L-AGE diet. Finally, mice on H-AGE diet had significantly fewer corpora lutea in their ovaries. These results indicate that the ingestion of high amounts of dietary AGEs could disrupt folliculogenesis and steroidogenesis that might lead to abnormal estrous cyclicity. Intake of dietary AGEs could also upregulate ovarian gene expression of inflammatory macrophage markers.

中文翻译：

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膳食高级糖化终产物（AGEs）可能会改变小鼠的卵巢功能。

营养是外源性AGE的重要来源，西式饮食中存在的热加工食品含有大量这些促炎性AGE。此外，饮食中AGEs的摄入可以上调炎症巨噬细胞标志物的卵巢基因表达。这项研究的目的是调查富含AGEs的饮食对小鼠模型中的发情循环和卵巢功能的影响。六周龄的C57BL / 6 J雌性小鼠随机接受AGEs低饮食（L-AGE）或AGEs高饮食（H-AGE），共13周。进行的实验包括每日阴道涂片以评估发情周期，卵巢超排卵以促性腺激素评估释放的卵母细胞数量，RT-PCR对整个卵巢组织mRNA定量，以量化参与卵泡生成，类固醇生成的基因，和巨噬细胞标志物，以及卵泡计数的卵巢形态。结果指标包括发情周期，超排卵后卵母细胞数量，卵泡发生，类固醇生成和巨噬细胞浸润相关基因的表达以及原始，初级，继发，窦房卵泡和黄体的数量。与接受L-AGE饮食的小鼠相比，接受H-AGE的小鼠在绝育期花费的时间明显更长，在卵巢超排卵后释放的卵母细胞数量相近，并且显示出与类固醇生成有关的基因发生了显着变化（Star mRNA表达水平增加）和卵泡形成（增加Gdf-9和Fshr mRNA表达水平）。与使用L-AGE饮食的小鼠相比，使用H-AGE饮食的小鼠中的小鼠巨噬细胞标记F4 / 80 mRNA表达上调。最后，H-AGE饮食的小鼠卵巢中的黄体明显减少。这些结果表明，摄入大量的饮食性AGEs可能会破坏卵泡生成和类固醇生成，从而可能导致发情周期异常。饮食AGEs的摄取也可以上调炎症巨噬细胞标记物的卵巢基因表达。