Severe Acute Respiratory Syndrome Corona Virus-2 (SARS-CoV-2), the zoonotic virus answerable for the current global health crisis is ringing its dangerous bells on its post disease status. COVID-19 is causing multiple organ damage probably with its entry site. Insulin-Dependent Diabetes (IDDM) also known as Type I Diabetes is a multifactorial disease that typically occurs as a result of the interaction of genetic, environmental and immunologic factors. The mechanisms behind the development of Diabetes and associated consequences are complicated. The morphological mass of Insulin producing β-cells in the pancreatic islets of Langerhans and the functional status determine plasma Insulin levels. Insufficient Insulin levels may develop as a result of a lack of β-cell function resulting in hyperglycemia and Diabetes. Angiotensin-Converting Enzyme 2 (ACE2) receptor, the binding agent which allows Corona virus to enter and migrate to various organs such as lungs, heart, liver, pancreas, and kidneys is assumed to be responsible for this damage. The over expression of ACE2 receptor on pancreatic endocrine cells paves a way for extensive damage to Islets of Langerhans causing Insulin resistance and deficiency. Another common assumption among the researchers and health care professionals are the dreadful relationship shared by viruses and Diabetes which can exacerbate or provoke autoimmunity leading to β-cell auto-oxidation. The metabolic complications like Diabetic Ketoacidosis (DKA) and Hyper osmolar hyperglycemia are predominantly seen in various regions of the world in people with Pre-Diabetes and non-diabetics. However, this review explored the probable truth behind COVID-19 induced new-onset Diabetes mellitus and its complications.
Key words: COVID -19, Type-1 Diabetes, ACE2 receptor, Diabetic, Ketoacidosis.
