Hyperinsulinemia of insulin resistance occurs because of a lack of vasodilatory and anti-inflammatory effects of insulin. It is not the insulin itself, but the loss of its anti-inflammatory effects due to insulin resistance that is the culprit in atherosclerosis of diabetes.1
Tseng2 states that the benefit of lowering blood glucose levels with exogenous insulin may be counteracted by the potential risk for insulin-induced atherosclerosis. Tseng2 frequently reiterates the atherogenic effects of insulin as if it were a proven fact. I find that the conclusion of this study, that insulin users are at higher risk for development of hypertension, is a speculation based on a flawed premise.
When comparing the users and nonusers of insulin, lipid profile was not measured in either group. Lipid status in people with type 2 diabetes mellitus is very relevant in assessing atherogenesis as an underlying cause for hypertension, whether insulin is . . . [Full Text of this Article]
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