Structural manifestations of diabetic cardiomyopathy in the rat and its reversal by insulin treatment

Abstract

The structural effects of diabetes and subsequent insulin treatment upon the contractile and supporting elements of the rat myocardium were examined at progressive stages of both untreated and treated disease. Diabetes was induced by intravenous injection of alloxan, and tissue was examined after 6, 12, and 26 weeks. Insulin treatment began after 12 weeks of diabetes and tissue from these animals was examined after the same intervals. Within the cardiocytes, diabetes produced a focal yet progressive loss of myofibrils, transverse tubules, and sarcoplasmic reticulum, and separation of the fasciae adherens was evident at the intercalated disk. Mitochondrial damage was not evident. These cytoplasmic alterations were accompanied by intercellular and perivascular deposition of connective tissue, thickening of the endothelial cytoplasm with pinocytotic hyperactivity, and characteristic basal laminar changes. When insulin treatment began after 12 weeks of diabetes, most, but not all, of these changes were reversed, and this reversal was essentially complete within 6-12 weeks. Even with longer periods of insulin treatment, cardiocytes still exhibited scattered areas of myofibril loss and extracellular matrix was retained. In contrast, diabetic changes in the intercalated disk and capillaries, including their basal laminae, were completely and rapidly reversed. It is hypothesized that the structural manifestations of diabetic cardiomyopathy consist of two major components; the first is a short-term, physiologic adaptation to metabolic alterations, while the other represents degenerative changes for which the myocardium has only a limited capacity for repair.

Taurine May Prevent Diabetic Rats from Developing Cardiomyopathy also by Downregulating Angiotensin II Type2 Receptor Expression

“…We used the standard for type 2 diabetic diagnoses in rats as follows: based on insulin resistance, a fasting blood sugar ≥16.7 mmol/L. Some reports indicate alteration of STZ-induced diabetic cardiomyopathic ultrastructure to take place from 8-12 weeks [9][10][11]. Cardiac function is altered in 6-14weeks [12], which seconded our observation.…”

Increase in albumin, IgG, and IgM blood-nerve barrier indices in human diabetic neuropathy.

“…This might be related to the endothelial hyperplasia observed in sural nerves from diabetics (16). It has also been demonstrated in heart capillaries that there is an increase in cytoplasmic vesicles in alloxan diabetes (35).…”

Alteration in Left Ventricular Diastolic Filling and Accumulation of Myocardial Collagen at Insulin-Resistant Prediabetic Stage of a Type II Diabetic Rat Model

“…It was likely that alteration in the diastolic function in the prediabetic stage was related to the remodeling of myocardial tissue structure. [21][22][23] The normal mitral flow velocity curve varies with age, loading conditions, and heart rate. 5 In our study, therefore, we age-matched our control rats, measured the blood pressure immediately after finishing Doppler echocardiography, and subclassified the OLETF rats and LETO rats according to their heart rate.…”