Currently, increasing attention has been paid to insulin resistance as a distinct cause of cardiac dysfunction, cardiomyopathy and heart failure (HF) in diabetic individuals. Therefore, the present study aims to explore the pathogenesis and reciprocal causal relationships between insulin resistance and cardiomyopathy/HF in two obese and non-obese insulin resistant animal models (SD rat). Here, we have created obesogenic diet (45% calorie from fat) induced obese, and atherogenic diet (4% cholesterol) with 10% fructose in drinking water induced non-obese animal models. Both obese and non-obese animals have developed insulin resistance syndrome compared to age-matched controls. Euglycemic-Hyperinsulinemic Clamp technique indicated that the obese animal exhibited insulin resistance (IR). In addition, obese rats accompany with hyperinsulinemia, activation of neurohumoral systems, concentric hypertrophy with slightly impairment of cardiac mechanical performance ( Pressure-Volume catheter), fewer changes in both plasma and myocardial metabolites profiling (LC-MS metabolites analysis) compared to non-obese IR rats. In contrast, less insulin resistance, hypoinsulinemia, hyperactivity of neurohumoral systems, eccentric hypertrophy with worse mechanical performance, robust changes in both plasma and myocardial metabolites profiling have been found in non-obese IR rats. In our animal models demonstrate that obese IR heart switched on the physiological adaptation and remodeling in the face of obese and insulin resistant stimuli. Whereas non-obese IR heart seems switched on the pathological adaptation and remodeling, and this adaptive eccentric hypertrophy was consequent detrimental to cardiac function. Our study indicated that insulin resistance but not obesity plays a pivotal role in development of cardiomyopathy. Insulin resistance disturbs systemic metabolic homeostasis may precipitate cardiac maladaptation and remodeling which may consequently lead to evolution of cardiomyopathy.