Type-2 diabetes used to be called non-insulin-dependent diabetes mellitus because, at least in the early stages of the disease, people do not require insulin treatment.
Unlike type-1 diabetes patients who have a fundamental failure of the insulin-producing beta cells of the islets of Langerhans in the pancreas and require insulin injections from the start, those with type-2 diabetes can still make insulin at diagnosis.
Conventional medical teaching has been that type-2 diabetes arises when the tissues become resistant to insulin. As a result, muscle and fat do not absorb sugar from the bloodstream, and the liver continues to produce glucose even when there is plenty being absorbed from food. As type-2 diabetes patients do not usually require insulin until they have had the disease for some years, and often not at all, it was assumed that their beta cells must be working relatively normally.
However, research has now shown that beta cell dysfunction and insulin resistance occur alongside one another. Patients who took part in the UK prospective diabetes study had already lost about 50 per cent of their beta cell function.
5And statisticians were able to calculate that deterioration had begun 12 years before diagnosis. Six years into the study and those on conventional treatment had lost a further 25 per cent of their beta cell function.
As Professor Tony Barnett, head of diabetology at Birmingham Heartlands Hospital, explains: 'We now know that there are two fundamental defects - insulin resistance and beta cell dysfunction - and both happen very early in the development of type-2 diabetes. In the past, beta cell function has been ignored but you don't get type-2 diabetes with insulin resistance alone.'