Insulin-Induced Toxicity Promotes Morphological and Biochemical Alterations in Cardiomyocytes

SUMMARY: Diabetic cardiomyopathy, commonly associated with insulin resistance and hyperinsulinemia, is characterized by impaired myocardial insulin signaling, mitochondrial dysfunction, endoplasmic reticulum stress, disrupted calcium homeostasis, altered coronary microcirculation, and maladaptive immune responses. These pathophysiological alterations contribute to oxidative stress, myocardial fibrosis, hypertrophy, diastolic dysfunction, and eventually systolic heart failure. In this study, cardiomyocytes of Rattus norvegicus were exposed to a high insulin concentration (10 IU/mL) for 6 hours. Inflammatory and oxidative stress markers were assessed, and cellular morphology was examined using May-Grünwald-Giemsa staining. High-dose insulin exposure significantly increased oxidative stress and inflammation, while reducing cell viability under hyperinsulinemic conditions. These findings indicate that insulin toxicity induces oxidative stress via reactive oxygen species generation and triggers inflammatory responses, highlighting its potential role in the pathogenesis of type 2 diabetes-associated cardiomyopathy.