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from SECTION 3 - MOLECULAR THERAPEUTICS
Published online by Cambridge University Press: 04 June 2019
INTRODUCTION
Diabetes mellitus is the commonest endocrine disorder across the globe. The rapid increase in the prevalence of obesity in both developed and developing countries has led to a concomitant rise in the number of subjects suffering from type 2 diabetes. There is strong epidemiological evidence that type 1 diabetes is also increasing in prevalence, but the reasons for this are currently unknown.
The two major forms of diabetes are thought to be separate entities, each with their own specific aetiology. Type 1 diabetes is an autoimmune disease, possibly initiated by viral infection, which leads to the complete destruction of the insulin-secreting beta cells in the islets of Langerhans of the pancreas. The aetiology of type 2 diabetes involves two metabolic flaws: resistance to the action of insulin, and failure of the insulin-secreting beta cells to produce sufficient insulin to counteract this resistance. The insulin resistance is often a direct result of obesity, while the molecular mechanisms involved in the beta cell secretory dysfunction, although well researched, are not yet fully understood.
The distinct aetiologies of the two diseases were also thought to be mirrored by differential susceptibility to the diseases based on age. The onset of type 1 diabetes was thought to be most common in childhood, and type 2 diabetes to be seen most frequently in subjects over the age of 40. However, epidemiological studies have shown that this distribution pattern is not inflexible. It has been found that older subjects do develop type 1 diabetes, and this form of adult-onset type 1 diabetes has been termed type 1.5 diabetes mellitus or latentautoimmune diabetes of adulthood (LADA). Also, type 2 diabetes is now being more commonly observed in children, a direct result of the increasing prevalence of obesity in this population group.
Recent years have seen major advances in the therapies used for treating both type 1 and type 2 diabetes. The use of genetic manipulation has allowed scientists to change the structure of the insulin molecule and hence design bio - engineered insulin that can be absorbed very quickly or very slowly. New therapies have also emerged for type 2 diabetes, by targeting the dysfunctional metabolic events that play a role in the disease aetiology.
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