Ultrastructure of heart muscle in short-term diabetic rats: influence of insulin treatment.
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.
D000138:Acidosis / Q000097:blood; D000643:Ammonium Chloride / Q000633:toxicity; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000473:pathology*; D006321:Heart / Q000187:drug effects; D049528:Insulin, Long-Acting / Q000494:pharmacology / Q000627:therapeutic use*; D007657:Ketone Bodies / Q000097:blood; D008297:Male; D008854:Microscopy, Electron; D009206:Myocardium / Q000648:ultrastructure*; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D049528:Insulin, Long-Acting; D007657:Ketone Bodies; D000643:Ammonium Chloride