Research suggests that postprandial hyperglycemia results in the activation of protein kinase-C in the endothelium, which increases the production of adhesion molecules, bringing more leukocytes into the blood vessels, thus creating more congestion and disrupting endothelial function. Also, high blood sugar has been found to increase platelet aggregation. All these mechanisms accelerate atherosclerosis. Another effect of elevated postprandial glucose is increased hypercoagulability, which comes from increased thrombin production and decreased fibrogen breakdown. All this results in increased blood clotting or hypercoagulability. Hypercoagulability facilitates atherosclerotic plaque. It appears that the control of postprandial hyperglycemia has been associated with some reversal of the hypercoagulable state. High glucose in the blood results in increased glycosylation of vascular proteins and also lipids in the arteries and endothelium. This results in glycated LDL particles, which are easily oxidized and taken up by the macrophages. This ... leads to higher foam cell production, which one gets with higher insulin levels. With higher foam cell production, there is more atherosclerotic plaque. The other mechanism by which glycation contributes to atherosclerosis is that the AGEs form in the collagen of the vessel wall and accelerate the atherosclerotic process. Gabriel Cousens, MD There Is a Cure for Diabetes Do you or someone you love suffer from Chronic Diabetes Degenerative Syndrome (a.k.a. NIDDM, IDDM, hypoglycemia, etc...)? Click here: ow.ly/v3Zqm
Posted on: Tue, 08 Apr 2014 14:01:18 +0000
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