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Insulin Increases The Transfer Of Glucose Into Cells Of The Liver, Skeletal ...


Insulin increases the transfer of glucose into cells of the liver, skeletal muscles and adipose tissue and is firstly used for energy needs and then glycogen is formed when energy needs have been satisfied. If there is still glucose left available then it is converted into fat and stored in the body.
Conversion for energy use is effected by transporter proteins called GLUT 4. These proteins are present in cytoplasmic vesicles and are inactive in the absence of insulin. Insulin stimulates the take up of amino acids by cells and promotes synthesis of fatty acids in the liver. Insulin increases protein synthesis and inhibits the breakdown of fat in adipose tissue (Nair, 2007, p185).
Type 1 diabetes is a rarer, less common type of diabetes and more often than not affects younger people. Type 1 diabetes usually begins before age 40 although there are exceptions. It is thought that the incidence and diagnosis of type 1 diabetes peaks around the age of 14 years. Type 1 diabetes is linked with a deficiency or complete lack of insulin (Sewell, 2007, p6). The aetiology of this disease is still as yet unknown. However, it is considered that the pancreatic islet cells stop producing insulin in the amounts needed to sustain a normal blood glucose level. Without sufficient insulin, blood glucose levels continue to rise, which can cause some of the common symptoms of hyperglycaemia (Nair, 2007, p186).
It is suggested that type 1 diabetes usually develops because of an autoimmune disorder. This is when the body's immune system starts to attack its own tissues as it would with any foreign tissue. For instance, in the case of type 1 diabetes, the islet beta cells of the pancreas that produce insulin are mistakenly perceived as the enemy. The body then generates antibodies to attack and destroy the foreign tissue and this in turn damages the islet beta cell's ability to produce insulin. Thereby, the deficiency of adequate insulin brings about diabetes. This is what has taken place in the pancreas of patient X. It is not known why this autoimmune diabetes develops, but scientists believe that there is a strong genetic predisposition (Atkinson & Eisenbarth, 2001, p222). It is proposed however, that the genetic propensity towards the disease might not be the solitary causative factor of type 1 diabetes. Environmental factors for example viral infections such as mumps, rubella, cytomegalovirus, measles, influenza, encephalitis, polio or Epstein-Barr virus have all been regarded as the aetiology of type 1 diabetes. Research has found that two individuals might be infected with an identical virus, but only one of them who could be genetically prone and go on to develop diabetes. Although why this happens is not fully known.

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