The type-1 diabetes is also called IDDM or insulin-dependent diabetes mellitus, as the patient must be treated (supplemented) with exogenous insulin, due to destruction of beta cells of pancreas which secrete insulin. As the insulin secreting beta cells are destroyed the pancreas (beta cells of pancreas) can not produce insulin and must be supplied from outside.

Autoimmune cause of type 1 diabetes:

The main cause of type diabetes is autoimmune (“immune-mediated form” of type I diabetes mellitus). Due to autoantibodies directed against the insulin secreting beta cells of pancreas, in the patient’s blood the beta cells are destroyed by the autoantibodies. The numbers of beta cells of pancreas are normal at the time of birth, but months or years after birth due to development of autoantibodies the destruction of beta cells of pancreas starts. The time taken for destruction of beta cells of pancreas may vary from patient to patient.

More than 95% of patient with type-1 diabetes develop the disease before 25 years of age. The onset of type 1 diabetes is usually acute (developing over a period of a few days to weeks). The acuteness of type 1 diabetes is destruction of more than 80% of beta cells of pancreas. The pancreas can maintain supply of insulin if beta cell mass of at least 20% is functioning and if the functional beta cell mass falls below 20% the clinical symptoms of diabetes develop.

Causes of type 2 diabetes are multifactorial and complex. Insulin resistance and abnormal insulin secretion are at the center to the development of type 2 diabetes. Many studies suggest that insulin resistance occurs before an insulin secretory defect and diabetes develops only when insulin secretion becomes inadequate. The genetic factor in development of type 2 diabetes is very strong in compare to type-1 diabetes. Environmental factors also play a strong role in causation of type-2 diabetes.

Genetic factor in causation of type 2 diabetes:

The genetic factor in causation of type 2 diabetes is very strong. The concordance of type 2 diabetes in identical twins is between 70% and 90%. If both parents have type 2 diabetes, the risk of development of type-2 diabetes among children is approximately 40%. Many first degree relatives of type-2 diabetes patients have reduced glucose utilization in skeletal muscles without diabetes, due to insulin resistance.

The types of diabetes with known causes are included and grouped in “other specific types of diabetes”. The “other specific types of diabetes” was previously known as MODY or maturity onset of diabetes of the young. The causes of “other specific types of diabetes” are several and varied and ranges from genetic defect to defect in insulin function to infection to drug or chemical-induced. The known causes of the “other specific types of diabetes” are discussed below.

Genetic defects of beta-cell function:

Diabetes due to genetic defect in beta-cell of pancreas function generally appears before the age of 25 years and with mild hyperglycemia. The genetic defect in beta-cell of pancreas function may be due to mutation in different (several) locations and mutation at different location causes different types of diabetes.

The exact cause of gestational diabetes in not clear and there is several theories which try to explain the cause of gestational diabetes, but gestational diabetes is not due to lack of insulin as is the case in type-2 diabetes, although the pathophysiologically is similar to type II diabetes.

Insulin resistance increases during pregnancy, may be due to blocking effects of other hormones on the insulin. Due to increase insulin resistance the secretion of insulin is increased to maintain the metabolism of glucose. The pregnant woman’s hunger increased due to increased insulin, eating more as a result. Increased level of insulin causes reduction of number of insulin receptors which increases the insulin resistance further, thus creating a vicious cycle.