IIS-Fundación Jiménez Díaz, Autónoma University, Avenue Reyes Católicos 2, 28040 Madrid, Spain ; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM) Network, 08017 Barcelona, Spain.
Mediators Inflamm. 2013;2013:461967. doi: 10.1155/2013/461967. Epub 2013 Oct 31.
Diabetic cardiomyopathy is initiated by alterations in energy substrates. Despite excess of plasma glucose and lipids, the diabetic heart almost exclusively depends on fatty acid degradation. Glycolytic enzymes and transporters are impaired by fatty acid metabolism, leading to accumulation of glucose derivatives. However, fatty acid oxidation yields lower ATP production per mole of oxygen than glucose, causing mitochondrial uncoupling and decreased energy efficiency. In addition, the oxidation of fatty acids can saturate and cause their deposition in the cytosol, where they deviate to induce toxic metabolites or gene expression by nuclear-receptor interaction. Hyperglycemia, the fatty acid oxidation pathway, and the cytosolic storage of fatty acid and glucose/fatty acid derivatives are major inducers of reactive oxygen species. However, the presence of these species can be essential for physiological responses in the diabetic myocardium.
糖尿病性心肌病是由能量底物的改变引发的。尽管血浆葡萄糖和脂质过多，糖尿病心脏几乎完全依赖于脂肪酸降解。脂肪酸代谢会损害糖酵解酶和转运蛋白，导致葡萄糖衍生物的积累。然而，与葡萄糖相比，脂肪酸氧化每摩尔氧产生的 ATP 产量更低，导致线粒体解偶联和能量效率降低。此外，脂肪酸的氧化可以饱和，并导致其在细胞质中沉积，在细胞质中，它们通过核受体相互作用偏离诱导有毒代谢物或基因表达。高血糖、脂肪酸氧化途径以及细胞质中脂肪酸和葡萄糖/脂肪酸衍生物的储存是活性氧的主要诱导剂。然而，这些物质的存在对于糖尿病心肌的生理反应可能是必不可少的。
