The Role Of Insulin Resistance And Hyperuricemia

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Insulin stimulates Ca-ATPase, Na-K-ATPase, and PI3K and decreases calcium influx into VSMC. Therefore, insulin resistance causes increased intracellular ionized calcium and reduced intracellular Mg ion concentration that has been associated with vasospasm, increased vascular reactivity, increased intracellular calcium concentration, the formation of pro-inflammatory agents, oxygen radicals, platelet aggregation, decreased cardiac bioenergetics, cardiac failure, lipoprotein oxidation, gender-related modulation of NO, increased vWF and oxygen free radical activity reflecting endothelial dysfunction and oxidative stress, and changes in membrane fatty acid saturation (11,77).

However, postprandial hyperinsulinemia is independently associated with CAD irrespective of fasting glucose, postprandial glucose, and fasting insulin levels in nondiabetic women with clustering of factors of the metabolic syndrome (78).

Insulin stimulates tumor necrosis factor (TNF)-a production in macrophages (79); TNF-a could play a role in the development of insulin resistance in humans, both in muscle and in vascular tissue (80).

The adipocyte-derived hormone, adiponectin, accumulates in the injured artery from the plasma and suppresses endothelial inflammatory response and VSMC proliferation, as well as macrophage-to-foam cell transformation in vitro. In Apo E KO mice, adiponectin treatment led to inhibition of lesion formation with smaller lipid droplets in the lesions, and suppressed mRNA of VCAM-1 and class A scavenger receptor (SR). Adiponectin migrates to foam cells in the fatty streak lesions (81).

Hyperuricemia, related to decreased renal blood flow, accompanies nephrosclerosis, predates proteinuria, and follow left ventricular hypertrophy. In the UKPDS, macrovascular and microvascular complications were reduced by BP and blood glucose control (82).

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