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首页> 外文期刊>American Journal of Physiology >Excess ω-6 fatty acids influx in aging drives metabolic dysregulation, electrocardiographs alterations, and low-grade chronic inflammation
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Excess ω-6 fatty acids influx in aging drives metabolic dysregulation, electrocardiographs alterations, and low-grade chronic inflammation

机译：老化的多余ω-6脂肪酸流入驱动代谢失调，心电图改变和低级慢性炎症

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摘要

Maintaining a balance of ω-6 and ω-3 fatty acids is essential for cardiac health. Current ω-6 and ω-3 fatty acids in the American diet have shifted from the ideal ratio of 2:1 to almost 20:1; while there is a body of evidence that suggests the negative impact of such a shift in younger organisms, the underlying age-related metabolic signaling in response to the excess influx of ω-6 fatty acids is incompletely understood. In the present study, young (6 mo old) and aging (≥ 18 mo old) mice were fed for 2 mo with a ω-6-enriched diet. Excess intake of ω-6 enrichment decreased the total lean mass and increased nighttime carbohydrate utilization, with higher levels of cardiac cytokines indicating low-grade chronic inflammation. Dobutamine-induced stress tests displayed an increase in PR interval, a sign of an atrioventricular defect in ω-6-fed aging mice. Excess ω-6 fatty acid intake in aging mice showed decreased 12-lipoxygenase with a concomitant increase in 15-lipoxygenase levels, resulting in the generation of 15(S)-hydroxyeicosatetraenoic acid, whereas cyclooxygenase-1 and -2 generated prostaglandin E_2, leukotriene B_4. and thromboxane B_2. Furthermore, excessive co-6 fatty acids led to dysregulated nuclear erythroid 2-related factor 2/antiox-idant-responsive element in aging mice. Moreover, ω-6 fatty acid-mediated changes were profound in aging mice with respect to the eicosanoid profile while minimal changes were observed in the size and shape of cardiomyocytes. These findings provide compelling evidence that surplus consumption of ω-6 fatty acids, coupled with insufficient intake of ω-3 fatty acids, is linked to abnormal changes in ECG. These manifestations contribute to functional deficiencies and expansion of the inflammatory mediator milieu during later stages of aging.
机译：保持ω-6和ω-3脂肪酸的平衡对于心脏健康至关重要。美国饮食中的电流ω-6和ω-3脂肪酸从2：1至近20：1的理想比率转移;虽然存在一系列证据表明这种转变对年轻生物的负面影响，但不完全了解响应于过量的ω-6脂肪酸的过流量的相关年龄相关的代谢信号。在本研究中，杨（6莫旧）和老化（≥18莫旧）小鼠用ω-6富含富含ω-6富含饮食。 ω-6富集的过量摄入量降低了总贫质量和增加的夜间碳水化合物利用率，具有较高水平的心肌细胞因子，表明低级慢性炎症。多谷氨酰胺诱导的应力测试显示了PR间隔的增加，ω-6喂养老龄化小鼠的房室缺陷的符号。在老化小鼠中的过量ω-6脂肪酸摄入量显示出12-脂氧合酶的增加，伴随着15-脂氧合酶水平的增加，导致产生15（S） - 羟基辛酸四烯酸，而环氧氧酶-1和-2产生的前列腺素E_2，白酮B_4。和血栓素B_2。此外，过量的CO-6脂肪酸导致衰弱的核红细胞2相关因子2 / Antiox-Idant响应性元素在老化小鼠中。此外，ω-6脂肪酸介导的变化在相对于果皮型曲线上的老化小鼠中深入，同时在心肌细胞的尺寸和形状中观察到最小变化。这些发现提供了令人信服的证据，即ω-6脂肪酸的剩余消耗与ω-3脂肪酸的摄入量不足，与ECG的异常变化有关。这些表现形式有助于在老龄化后期阶段的炎症调解员Milieu的功能缺陷和扩张。

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