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From India:

"Arterial muscle tone forces arterial wall muscle to relax, increasing blood flow, especially in micro arteries; lack of insulin reduces flow by allowing these muscles to contract," according to the Wikipedia encyclopedia. If this action of insulin is correct, then can persistent hyperglycemia, excess of other bio-substances in blood, such as sodium, cause the hypotonicity/thinning of blood making blood cells swell or deficiency of insulin and cause vasoconstriction? Can such vasoconstriction affect diffusion or leaking of glucose and insulin from vascular compartments into target tissues resulting in hyperglycemia and insulin resistance?

Medicated insulin secretion and injected insulin may keep the continuous presence of insulin in blood whereas normal secretion of insulin may not. Can such continuous presence of insulin encourage persisting vasodilation and maybe damage to vascular walls?


Remember that most glucose transport in the fasting state is not dependant on insulin. However, during the post-absorptive state, when insulin is secreted in response to the rising glucose, insulin is normally produced. This causes insulin-mediated vasodilation in muscle and recruits tissues for glucose uptake. Insulin resistance may indeed play a role in the inability to recruit muscle tissue for glucose disposal. However, it is not necessarily persistent insulin that is necessary.


Original posting 26 May 2006
Posted to Other and Insulin


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