Semantron 2014

one study were insulin-independent after one year. 10

cell transplantation cannot be an effective widespread cure for type 2 diabetes.

The current ineffectiveness of this treatment may be due to the effects of the immunosuppressant drugs used to prevent the islet cells from being rejected. Calcineurin inhibitors and Sirolimus (both commonly used to prevent rejection of organ transplants) can impair islet cell function and also decrease the bodyÊs sensitivity to insulin, causing diabetes-like symptoms. 11 This is rather ironic as the drugs needed to prevent the body from rejecting the islet cells can also cause the transplanted islet cells to fail. A second adverse effect of immunosuppressant drugs, particularly calcineurin inhibitors, is that they are nephrotoxic (poisonous to the kidneys). Most patients are able to tolerate the drugs reasonably well and as a result their kidney function will slowly improve after the initial toxicity. However some patients, particularly those with pre-existing kidney problems, may experience complete renal failure as a direct result of the immunosuppressant drugs, which results in the patient needing a kidney transplant to survive. In addition to these problems, islet cell transplants currently require 2 donor pancreases for every treatment. In conclusion, Islet cell transplantation is a relatively successful method for treating type 1 diabetes. However, it poses similar risks to whole pancreas transplants, with the addition risk of the islet cells failing. However the reduced immunosuppressant drug regime used in islet cell transplantation poses a lower risk of infections than a whole pancreas transplant over the long term. Therefore, islet cell transplantation is a very promising cure for type 1 diabetes, especially as new stem cell research may make it possible to artificially produce islet cells of the patientÊs exact tissue type. Despite this, without further development in immunosuppressant drugs or methods to make more donor pancreases available, islet 10 http://www.transplantation-proceedings.org/article/S0041- 1345(04)01555-6/abstract . 11 http://care.diabetesjournals.org/content/26/12/3288.

Type 2 diabetes is the most prevalent form of diabetes and develops in adults. It is a disease which causes tissues to become insulin resistant. This means the tissues will not respond to the normal amounts of insulin produce by the pancreas. Type 2 diabetes is also characterized by relative insulin deficiency. 12 One of the main factors believed to cause type 2 diabetes is a personÊs weight. Studies have shown that obesity is associated with 60-80% of cases of type 2 diabetes in Caucasian adults. It is believed that carrying excess fat causes the body to store some of these lipids in inappropriate places such as the heart, the liver and blood vessels. When this occurs, the probability of developing insulin resistance increases dramatically. Although this link has been proven, the science and reasoning behind it is uncertain. If we were able to prevent fat from accumulating in inappropriate parts of the body then we could potentially stop type 2 diabetes developing as a result of obesity and to some extent reverse pre-existing diabetes which was originally caused by excess weight. Scientists in Sweden have identified a protein called VEGF-B which is involved in the storage of fat in the body. It was thought that perhaps inhibiting this protein, using the monoclonal antibody 2H10, would prevent obesity from being a major causal factor for type 2 diabetes. Studies to prove this effect were then carried out using normal mice. These mice were made obese using a high fat diet and then allowed to develop type 2 diabetes. Once treated with 2H10, the miceÊs diabetes was reverse to various extents, allowing glucose levels to be controlled without insulin therapy. In addition, mice which were in the process of developing diabetes as a result of their obesity were also treated with 2H10, which stopped the natural onset of diabetes. This 12 http://en.wikipedia.org/wiki/Diabetes_mellitus_type_2 #cite_note-Pathologic_Basis_of_Disease-2.

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