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Diabetes breakthrough

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liambob1    1

I was reading about a recent breakthrough by the fine folks at Trinity college here in Ireland, the article in question says that A hormone called Amylin, or Islet Amyloid Polypeptide (IAPP) has been discovered to a key underlying cause to type two diabetes and the main trigger for the disease because it gets deposited in the pancreas and causes the body to produce much greater levels of insulin than it normally would. It is claimed that a drug could be designed to suppress this hormone and thus bring insulin levels back down and prevent the onset of diabetes, My question is that would the suppression of this hormone have any serious adverse effects or cause any other complications.


A brief discription of the article is available here

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Marat    239

Several things happen in type 2 diabetes: First, the cell walls throughout the body become resistant to the entry of insulin, and in response, the pancreas produces more and more insulin to overcome the resistance. Second, as the ability to overcome this resistance declines with the increasing exhaustion of the pancreas by constantly having to over-produce insulin, the blood sugar rises. This is why patients can begin their therapy with diet and excercise, but then have to add oral medications, and finally have to start injecting insulin. The third process is that either the hyperglycemia itself, the atherogenic properties of excess insulin flowing through the vascular system, an inflammatory process that occurs along the inner walls of the vascular system, genetic predispositioning, or some combination of all four phenomena occurs to cause the vascular and neurological complications of the disease.


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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