Posted 13 September 2010 - 12:48 PM
A brief discription of the article is available here
Posted 13 September 2010 - 10:08 PM
The amylin deposits on the pancreas described here may only be a side-effect rather than an important step in the causality of the processes of pancreatic beta cell destruction. Even if it is part of the causal mechanism by which the ability of the pancreas to produce insulin is destroyed, blocking this step would not address the initial mechanism which causes the disease, which is the increased resistance to the passage of insulin at the cell walls. So if blocking this step prevented or slowed the pancreatic burn-out, the cell wall resistance to insulin would persist, and you would still have type 2 diabetics suffering excess insulin production all the time, and having supra-physiological levels of insulin floating around all the time is damaging to the cardiovascular system, and the hyperglycemia from the inability of the insulin to transport glucose across the cell walls would also continue.
Also, by far the worst form of the disease, the autoimmune condition of type 1 diabetes, might not be addressed. I say 'might not' because it has recently been suggested that type 1 and type 2 diabetes may both be autoimmune diseases, so if the amylin plays a role in the autoimmune apoptosis of the pancreatic beta cells, perhaps this new result could suggest a line of intervention less toxic than immunosuppressive drugs to prevent or at least delay type 1 diabetes.
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