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首页> 外文期刊>Life sciences >Chronic ingestion of a Western diet increases O-linked-β-N- acetylglucosamine (O-GlcNAc) protein modification in the rat heart
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Chronic ingestion of a Western diet increases O-linked-β-N- acetylglucosamine (O-GlcNAc) protein modification in the rat heart

机译：长期摄入西方饮食会增加大鼠心脏中O-β-N-乙酰氨基葡萄糖（O-GlcNAc）蛋白的修饰

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Aims: Protein O-GlcNAcylation is both a nutrient sensing and cellular stress response that mediates signal transduction in the heart. Chronically elevated O-GlcNAc has been associated with the development of cardiac dysfunction at both the cellular and organ levels in obesity, insulin resistance and diabetes. Development of these pathologies is often attributed to diets high in saturated fat and sugar (a "Western" diet; WES) but a role for O-GlcNAc in diet-induced cardiac dysfunction has not been established. The aims of this study were to examine the effect of chronic consumption of WES on cardiac O-GlcNAcylation and investigate associations of O-GlcNAc with cardiac function and markers of cellular stress. Main methods: Young male rats received either a control diet (CON; n = 9) or WES (n = 8) diet for 52 weeks. Key findings: There was no evidence of cardiac dysfunction, advanced glycation endproduct (AGE) accumulation, pathological cardiac hypertrophy, calcium handling impairment, fibrosis or endoplasmic reticulum stress in WES hearts. However, cardiac O-GlcNAc protein, particularly in the higher molecular weight range, was significantly higher in WES hearts compared to CON (P < 0.05). Protein levels of the enzymes that regulate O-GlcNAc attachment were not different between groups; thus, the increased O-GlcNAcylation in WES hearts appears to be due to increased nutrient availability rather than enzymatic regulation of cellular stress. Significance: These data suggest that diets high in saturated fat and sugar may contribute to the adverse effects of metabolic syndrome and diabetes by an O-GlcNAc-mediated process and that this may occur in the absence of overt cellular stress.
机译：目的：蛋白质O-GlcNAcylation既是营养素感应，又是细胞应激反应，介导心脏中的信号转导。 O-GlcNAc的长期升高与肥胖，胰岛素抵抗和糖尿病的细胞和器官水平的心脏功能障碍的发展有关。这些病理的发展通常归因于饱和脂肪和糖含量高的饮食（“西方”饮食; WES），但尚未确定O-GlcNAc在饮食引起的心脏功能障碍中的作用。这项研究的目的是检查长期服用WES对心脏O-GlcNAcy的影响，并研究O-GlcNAc与心脏功能和细胞应激标志物的关系。主要方法：年轻雄性大鼠接受对照饮食（CON; n = 9）或WES（n = 8），持续52周。主要发现：在WES心脏中，没有心脏功能障碍，晚期糖基化终产物（AGE）积累，病理性心脏肥大，钙处理障碍，纤维化或内质网应激的证据。然而，与CON相比，在WES心脏中的心脏O-GlcNAc蛋白（特别是在较高分子量范围内）显着更高（P <0.05）。两组之间调节O-GlcNAc附着的酶的蛋白质水平没有差异。因此，在WES心脏中增加的O-GlcNAcylation似乎是由于营养物质的增加而不是酶对细胞应激的调节。启示：这些数据表明，高饱和脂肪和糖的饮食可能是由O-GlcNAc介导的过程导致的代谢综合症和糖尿病的不良反应，并且这可能在没有明显的细胞应激的情况下发生。

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