**7. Beta cell dysfunction and apoptosis**

**Type one diabetes:** Islet beta-cells are almost completely destroyed when patients with type 1 diabetes are diagnosed. Type 1 diabetes occurs when the bodies own immune system de‐ stroys the beta cells. Some people develop a type of diabetes – called secondary diabetes - which is similar to type 1 diabetes, but the beta cells are not destroyed by the immune system but by some other factor, such as cystic fibrosis or pancreatic surgery.

**Type two diabetes:** Defects in insulin action and insulin secretion are both present in type 2 diabetes, and both are believed to be genetically predetermined. In the absence of a defect in beta-cell function, individuals can compensate indefinitely for insulin resistance with appro‐ priate hyperinsulinemia, as observed even in obese populations. Both insulin secretion and insulin action are impaired in type 2 diabetes. However, when allowance is made for the hy‐ perglycaemia and the fact that glucose stimulates insulin secretion, it becomes apparent that the insulin levels in diabetic patients are lower than in healthy controls and inadequate betacell function therefore represents a key feature of the disease. Theoretically, the insulin se‐ cretory defect could result from either defects of beta-cell function or a reduction in beta-cell mass. Most quantitative estimates indicate that type 2 diabetes associates with either no change or < 30% reduction in beta-cell mass. Moreover, the secretion defect is more severe than can be accounted for solely by the reduction in beta-cell mass. It therefore appears that the insulin secretory defect in type 2 diabetes does not primarily result from insufficient be‐ ta-cell mass but rather from an impairment of insulin secretion.
