Wednesday, January 27, 2010

What Is Diabetes?

Diabetes occurs either because of a lack of insulin or because of the presence of factors that oppose the action of insulin. The result of insufficient action of insulin is an increase in blood glucose concentration (hyperglycaemia). Many other metabolic abnormalities occur, notably an increase in ketone bodies in the blood when there is a severe lack of insulin.

There are the types of diabetes: Type 1 diabetes (previously insulin dependent diabetes) is due to B-cell destruction, usually leading to absolute insulin deficiency). It can be immune mediated or idiopathic. Type 2 diabetes (previously non-insulin dependent diabetes) ranges from those with predominant insulin resistance associated with relative insulin deficiency, to those with a predominantly insulin secretory defect with insulin resistance.

Type 1 and Type 2 diabetes are the commonest forms of primary diabetes mellitus. The division is important both clinically in assessing the need for treatment, and also in understanding the causes of diabetes which are entirely different in the two groups.


• Type 1 diabetes
Type 1 diabetes is due to destruction of B-cells in the pancreatic islets of Langerhans with resulting loss of insulin production. A combination of environmental and genetic factors that trigger an autoimmune attack on the B-cells is responsible, occurring in genetically susceptible individuals.
Thus, among monozygotic identical twins only about one-third of the pairs are concordant for diabetes in contrast to the situation in Type 2 diabetes where almost all pairs are concordant. The process of islet destruction probably begins very early in life and is known to start several years before the clinical onset of diabetes.
• Type 2 diabetes
There are numerous causes of Type 2 diabetes, which is now known to include a wide range of disorders with differing progression and outlook. The underlying mechanism is due either to diminished insulin secretion—that is, an islet defect, associated with increased peripheral resistance to the action of insulin resulting in decreased peripheral glucose uptake, or increased hepatic glucose output.
Probably as many as 98% of Type 2 diabetic patients are “idiopathic”—that is, no specific causative defect has been identified. Whether decreasing insulin secretion or increasing insulin resistance occurs first is still uncertain, but the sequence of events may vary in different individuals. Obesity is the commonest cause of insulin resistance. Some adults (especially those not overweight) over 25 years of age who appear to present with Type 2 diabetes may have latent autoimmune diabetes of adulthood (LADA) and become insulin dependent. Autoantibodies are often present in this group of patients.
Type 2 diabetes is a slowly progressive disease: insulin secretion declines over several decades, resulting in an insidious deterioration of glycaemic control which becomes increasingly difficult to achieve


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