Abstract *Corresponding author Frank Christopher Howarth, Department of Physiology, College of Medicine & Health Sciences, P.O. Box 17666, Al Ain, UAE University, UAE, Tel: 0097137137536; Email: Submitted: 16 September 2017 Accepted: 28 September 2017 Published: 29 September 2017 Copyright © 2017 Howarth et al. OPEN ACCESS Keywords • Streptozotocin • Diabetes mellitus • Rat • Cardiomyopathy • Heart • Ventricle • Calcium signaling • Contraction Diabetes mellitus (DM) is a major global health disorder currently affecting 450 million people. Diabetic cardiomyopathy (DC) is a disorder of cardiac muscle that is independent of coronary artery disease and that may lead to heart failure in diabetic patients. The precise mechanism(s) of diabetic cardiomyopathy are still not fully understood. Therefore, it is of paramount importance to develop experimental models of DM to study the time course and cellular, subcellular and molecular mechanisms of diabetic cardiomyopathy. With this in mind, scientists initially discovered that the antibiotic, streptozotocin (STZ) could be used to rapidly to induce diabetes mellitus in animal models. STZ destroys pancreatic beta cells, leading to hypoinsulinemia and hyperglycaemia. If left untreated hyperglycaemia may lead to DC and eventually heart failure. Initially in DM, the cardiac myocytes become apoptotic, disorganised and the number of myocytes are significantly reduced. The heart responds by enlarging itself (hypertrophy) which is accompanied by fibrosis leading to a physiological remodelling process. Within the myocytes, the process of excitation-contraction coupling (ECC) is deranged. This is due to an inability of the heart cells to regulate Ca2+ which is the initiator and regulator of cardiac muscle contraction. As a result, the heart takes longer to contract and to relax leading to DC, progressive heart failure and eventually sudden cardiac death. The aim of this review was to evaluate our current understanding of contractile dysfunction and disturbances in Ca2+ transport in the STZ-induced diabetic rat heart