Diabetes Mellitus type 1 is characterised by the reduced production of insulin. This can be attributed to the fact that type 1 is an autoimmune disorder in which the body’s own immune system attacks the glutamate decarboxylase enzyme in the hormone producing beta cells of the Islets of Langerhans in the pancreas. Thus stopping the production of insulin and results in a hyperglycaemic state. The autoimmune attack is generally triggered by an infection often a virus. This expresses a protein, which is similar to glutamate decarboxylase and leads to molecular mimicry thus the immune system destroys the insulin producing beta cells in the pancreas mistaking them for the virus.
In type 2 Diabetes Mellitus the pancreas continues to produce insulin, however a resistance to it occurs in body cells. Cells such as the muscle and liver cells that require insulin to permit the take up of glucose from the blood are unable to do so, resulting in a relative insulin deficiency. The main characteristics of this disease are 1) decreased insulin secretion 2) increased lipolysis (the hydrolysis of lipids) 3) increased hepatic glucose production (gluconeogenesis – the conversion of fat, protein and lactate molecules into glucose by the liver.) 4) decreased muscular glucose uptake. All these contribute to the development of hyperglycaemia, which often goes unnoticed for years. Diabetes Mellitus type 2 seems to be genetically inherited, although other factors such as obesity increase the risk of developing it.
The first symptoms of diabetes are related to the direct effects of Hyperglycaemia. When blood sugar levels rise above 160-180 mg/dL glucose passes into the urine and the kidneys excrete additional water to dilute the large amounts of glucose resulting in abnormal thirst (polydipsia).
Diabetic ketoacidosis is an acute dangerous complication far more common in diabetes type 1 than type 2. It begins when insulin levels are low, even if high levels of glucose are present in the blood, cells are unable to use it due to the lack of insulin thus they turn to other sources of energy. Fat cells are broken down in the liver producing ketones, which are acidic and lower the pH of the blood resulting in nausea, fatigue, vomiting and abdominal pain. Breathing becomes deep and rapid as the body attempts to correct the blood’s pH, a sign is when the persons breath smells of acetone without treatment this can progress into a diabetic coma.
Long term effects of Diabetes Mellitus include damage to small blood vessels (microangiopathy). Distinct types of this are diabetic neuropathy and retinopathy, the damage in both these cases seem to be linked to high glucose levels, which seem to have changed the behaviour of various proteins and so the tissues they are present in.
Peripheral neuropathy is caused by damage to the nerve fibres which affects sensation in the feet and lower legs and eventually in the fingers and hands, as feeling decreases so does reaction to damage e.g. Blisters, burns and cuts combined with slower healing thus increasing the risk of serious infection. Diabetic retinopathy is caused by damage to small blood vessels in the retina by high glucose levels. Initially these vessels become leaky, and may become blocked leading to several other difficulties such as swelling in the blood vessels resulting in haemorrhaging of the retina. Alternatively blocked vessels starve the retina of oxygen causing growth of abnormal growth of vessels in the retina. Both of these conditions can lead to blindness.
