Diabetes is a term given to a group of metabolic diseases characterised by high blood glucose levels (hyperglycermia) that are caused by defects in insulin secretion, insulin activity, or both. There are 2 main types of diabetes, type 1 and type 2 which affects c. 8% and 90% respectively of those with diabetes. Other forms include gestational diabetes, genetic conditions affecting β-cell action or insulin action etc.
Type 1 diabetes is, for the vast majority of cases, an autoimmune condition whereby the body’s immune system attacks the β-cells in the pancreas preventing the secretion of insulin. Due to the lack of insulin, whilst the body will continue to break down carbohydrates into glucose, it is not able to enter cells and be utilised, leading to high blood sugar levels.
Markers of the immune destruction of the β-cells include islet cell autoantibodies, autoantibodies to insulin, autoantibodies to GAD65 and autoantibodies to the tyrosine phosphatases IA-2 and IA-2β. One or more of these autoantibodies are present in 85 – 90% of cases.
In individuals suffering from type 2 diabetes, the pancreas still produces insulin, but not at sufficient levels to maintain blood glucose. High circulating blood glucose levels trigger the pancreas to produce more insulin to attempt to lower the glucose levels. In some individuals, this can eventually affect the pancreas causing it to produce less insulin which leads to even higher blood glucose levels and increasing risk of hyperglycaemia.
Chronic hyperglycaemia found in those with diabetes is associated with dysfunction of several different organs including eyes, kidneys, heart and blood vessels.