ABSTRACT
Diabetes mellitus is defined by a fasting blood glucose concentration≥7.0 mmol/L or an abnormal rise in blood glucose following an oral load. The two commonest forms are type 1 (insulin dependent) diabetes, which has a strongly inherited predisposition and variable annual incidence in different countries (~1 to 2 per 100,000 in Japan, >40 per 100,000 in Finland), and type 2 (non-insulin dependent) diabetes, which also has a strong inherited component and is much commoner than type 1 (Wolff, 1993). Type 1 diabetes is caused by an autoimmune destruction of the islets of Langerhans following an environmental insult (e.g. infection with Coxsackie virus) in genetically predisposed individuals. Patients with type 1 diabetes have a near total loss of insulin secretion, which results in increased glycogen metabolism, elevated circulating plasma glucose levels and ketoacidosis. Type 2 diabetes is more complex and in these patients hyperglycaemia is associated with varying degrees of insulin resistance and relative impairment of insulin secretion (Jaap et al., 1994). Insulin secretion declines with age and thus type 2 diabetes is increasing in our ageing population. In contrast to untreated type 1 diabetes, where circulating concentrations of insulin are low or absent, the plasma concentrations of insulin in type 2 diabetics may in the early stages of the disease be higher than in non-diabetic subjects. However, blood glucose is elevated due to impaired responses to insulin either at or beyond the level of the insulin receptor.
