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首页> 外文期刊>American Journal of Physiology >Sex modifies the consequences of extended fructose consumption on liver health, motor function, and physiological damage in rats.
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Sex modifies the consequences of extended fructose consumption on liver health, motor function, and physiological damage in rats.

机译：性改变大鼠肝脏健康，运动功能和生理损伤的裂变消耗的后果。

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Sex differences are evident in the presentation of metabolic symptoms. A shift of sex hormones that signal the onset of puberty combined with a poor diet consumed in adolescence is likely to have sex-specific, long-term impacts on adult physiology. Here, we expanded on existing literature to elucidate the sex-specific mechanisms driving physiological deficits following high fructose consumption. Male and female Wistar rats were fed a high-fructose (55%) diet beginning immediately postweaning for 10 wk. Female rats fed the high-fructose diet displayed elevated weight gain and extensive liver pathology consistent with markers of nonalcoholic fatty liver disease (NAFLD). Male rats fed the high-fructose diet exhibited increased circulating glucose along with moderate hepatic steatosis. Levels of cytokines and gene expression of inflammatory targets were not altered by fructose consumption in either sex. However, circulating levels of markers for liver health, including alanine transaminase and uric acid, and markers for epithelial cell death were altered by fructose consumption. From the alterations in these markers for liver health, along with elevated circulating triglyc-erides, it was evident that liver health had deteriorated significantly and that a number of factors were at play. Both adult fructose-fed male and female rats displayed motor deficits that correlated with aberrant structural changes at the neuromuscular junction; however, these deficits were exacerbated in males. These data indicate that consumption of a high-fructose diet beginning in adolescence leads to adult pathology that is modified by sex. Identification of these sex-specific changes has implications for treatment of clinical presentation of metabolic syndrome and related disorders.
机译：在代谢症状的介绍中，性差异是显而易见的。性激素的转变，信号发出青春期消耗的贫困饮食的发作，可能对成年生理学产生性别特异性，长期影响。在这里，我们扩大了现有文献，以阐明在高果糖消耗后促进生理缺陷的性别特定机制。男性和女性Wistar大鼠喂养高果糖（55％）饮食，开始于10周的10周。喂养高果糖饮食的雌性大鼠呈现升高的重量增益和广泛的肝脏病理，与非酒精性脂肪肝疾病（NAFLD）的标志物一致。喂养高果糖饮食的雄性大鼠表现出循环葡萄糖以及中度肝脏脂肪变性。炎症靶点的细胞因子和基因表达的水平未通过两性果糖消耗来改变。然而，通过果糖消耗改变了肝脏健康的循环水平，包括丙氨酸转氨酶和尿酸，以及上皮细胞死亡的标记。从这些标志物中的改变，对于肝脏健康，随着升高的循环三曲艾尔德，很明显，肝脏健康状况显着恶化，并且许多因素在发挥作用。成人果糖喂养的男性和雌性大鼠均显示出与神经肌肉交界处的异常结构变化相关的电机缺陷;然而，这些缺陷在雄性中加剧了。这些数据表明，在青春期开始的高果糖饮食的消耗导致成年病理学，其被性别修饰。鉴定这些性别特异性变化对治疗代谢综合征和相关疾病的临床表现有影响。

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