Higher than normal glucose levels are results of defective insulin secretion, insulin action or both. The pathology of type 1 disease involves islet cell destruction and beta-cell loss (two types of cells in the pancreas responsible for making and secreting insulin) leading to an absolute lack of insulin. It is believed that cytotoxic T lymphocytes and macrophages which are types of immune cells, target the destruction of islet cells possibly due to viral causes, toxins, or autoimmune stimulation.
In contrast, the size and number of beta cells are relatively normal in type 2 disease. The number of beta cells may even be increased due to a compensatory mechanism of the pancreas to secrete more insulin as a response to a state of insulin resistance. In addition, the liver of a patient with type 2 diabetes may be producing too much glucose or the timing of insulin secretion is inappropriate.