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胰岛素抵抗时心肌代谢重构,葡萄糖摄取及利用减少,脂肪酸生成和摄取过多,使得心肌细胞内游离脂肪酸(FFA)含量显著高于正常心肌。早期脂肪酸β氧化相关的酶表达及活性增加,对FFA氧化利用同时也增加。晚期参与脂肪酸氧化的基因下调或功能缺陷,FFA氧化利用减少,直接造成三磷酸腺苷(ATP)缺乏,包括离子泵、复极钾电流、ATP敏感性钾电流在内的心肌功能受限。并间接造成心肌细胞内FFA含量过多、钙超载、糖酵解中间产物聚集、氧应激异常等不良反应。在链脲酶素大鼠心室肌观察到瞬时外向钾电流密度显著下降,而应用胰岛素能短暂促进葡萄糖利用,逆转这一改变。提示离子通道功能与细胞能量供应和代谢存在关系。
Insulin resistance myocardial metabolism remodeling, glucose uptake and utilization decreased, fatty acid production and uptake, making the content of free fatty acids (FFA) in myocardial cells was significantly higher than normal myocardium. Early fatty acid β-oxidation-related enzyme expression and activity increased, while the use of FFA oxidation also increased. Late involvement of genes involved in fatty acid oxidation is downregulated or dysfunctional, with reduced FFA oxidation and a direct deficiency of adenosine triphosphate (ATP), with limited myocardial function including ion pump, repolarization potassium current, and ATP-sensitive potassium current. And indirectly cause myocardial FFA excessive content of cells, calcium overload, glycolytic intermediates aggregation, abnormal oxygen stress and other adverse reactions. In streptozotocin-induced rat ventricular muscle, transient outward potassium current density was significantly decreased, while insulin was used to transiently promote glucose utilization, reversing this change. Suggesting that ion channel function and cell energy supply and metabolism are related.