Reinilä A, Akerblom H K
Diabetologia. 1984 Sep;27(3):397-402. doi: 10.1007/BF00304857.
The ultrastructure of myocardium was examined in short-term diabetic rats. Morphometric analysis showed the volume of myocytic mitochondria, sarcoplasmic reticulum and lipid droplets to be significantly increased compared with those of control animals. Further measurements of mitochondria and sarcoplasmic reticulum indicated that the augmentation of these compartments was accountable by the enlargement of pre-existing mitochondria, which were swollen, and of pre-existing tubules of sarcoplasmic reticulum, the lumen of which was dilated. After insulin treatment the morphological changes were returned to normal which indicates that they were not due to the toxic effect of streptozotocin but were caused by the diabetic state per se. This suggestion is further supported by the finding that experimentally induced metabolic acidosis without diabetes did not cause any morphologically detectable changes in the heart muscle. It is concluded that short-term diabetes in the rat causes mitochondrial swelling, dilatation of sarcoplasmic reticulum and accumulation of lipid in cardiac myocytes, and that these changes are preventable with insulin treatment. We suggest that insulin may have an important role in the maintenance of metabolism in heart muscle.
对短期糖尿病大鼠的心肌超微结构进行了检查。形态计量分析显示，与对照动物相比，心肌细胞线粒体、肌浆网和脂滴的体积显著增加。对线粒体和肌浆网的进一步测量表明，这些细胞器的增大是由于原有线粒体肿胀以及原有肌浆网管腔扩张所致。胰岛素治疗后，形态学变化恢复正常，这表明这些变化并非由链脲佐菌素的毒性作用引起，而是由糖尿病状态本身所致。实验性诱导的无糖尿病代谢性酸中毒未引起心肌任何形态学上可检测到的变化，这一发现进一步支持了这一观点。结论是，大鼠短期糖尿病会导致心肌细胞线粒体肿胀、肌浆网扩张和脂质蓄积，而胰岛素治疗可预防这些变化。我们认为胰岛素可能在维持心肌代谢中起重要作用。
