Type I diabetes mellitus was formerly called Insulin-Dependent Diabetes Mellitus (IDDM) or juvenile diabetes, as most (more than 95%) of the patients with type I diabetes develop the disease before the age of 25 years. Type I diabetes is an autoimmune disease and autoimmune reaction/process leads to destruction of ? (beta) cells of pancreas, which secrete insulin and lead to absolute insulin deficiency.

The incidence of type 1 diabetes is same in both sexes (males and females). Type 1 diabetes is more common among white race (Caucasoid population). In type I diabetes, a family history of type 1 diabetes mellitus, gluten enteropathy or celiac disease or other endocrine diseases can commonly be present.

The onset of type I diabetes is acute (unlike type II diabetes which starts slowly) which develop over a few days to weeks. Most patients with type I diabetes have antibodies to islet cells of pancreas and called “immune-mediated form” of type I diabetes. Some type I diabetes patients have no antibodies to islet cells of pancreas and are called “idiopathic form” of type I diabetes and generally of African or Asian origin and are more prone to ketosis.

Type 1 diabetes results due to complex interaction between genetic, environmental, and immunologic factors. The ultimate result of these genetic, environmental, and immunologic interaction leads to destruction of the pancreatic beta cells and insulin deficiency, which in many cases are absolute. Until approximately 80% of beta cells of pancreas are destroyed the symptoms of diabetes do not become evident. The point from where diabetes become evident in type I diabetes, some residual activity (secretion of insulin) still exists among beta cells, although the insulin is insufficient for glucose metabolism.

A “honeymoon” phase occurs in type I diabetes, after the initial presentation of diabetes, when the insulin requirement is low (can be managed with small quantity of insulin) and in rare cases insulin is not required. But this “honeymoon” phase do not last long as the remaining beta cells are destroyed by autoimmune process and the type I diabetes patient becomes completely dependent on exogenous insulin.