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Part of the book series: Proteins And Cell Regulation ((PROR,volume 6))

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Abstract

Risk factors for coronary heart disease (CHD) include decreased insulin sensitivity and glucose intolerance, hypertension, increased body fat mass, unfavorable body fat distribution, the prothrombotic state and dyslipidemia. A clustering of these metabolic disturbances is also seen in Insulin Resistance and the metabolic syndrome. It has been shown that lipoproteins, triglycerides (TG), fatty acids and glucose can activate endothelial cells most likely due to the production of reactive oxygen species (ROS). Elevation of TG, fatty acids and glucose are common disturbances in the metabolic syndrome and are most prominent in the postprandial phase. Furthermore, postprandial lipemia has been associated with decreased HDL-C concentrations. The postprandial phase is therefore considered to be a pro-atherogenic and pro-oxidative condition. Paraoxonase 1 (PON1) is a HDL-associated enzyme with the ability to hydrolyze oxidized lipids, reducing oxidative stress in lipoproteins and in macrophages. Postprandial HDL-C decrease is associated with a decrease of PON1 activity. Subjects at risk for CHD, such as type 2 diabetics and patients with hypercholesterolemia have low PON1 activity. Furthermore, expression of PON1 inhibits the development of atherosclerosis in mice. Classic determinants of postprandial lipemia such as fasting TG, apolipoprotein B (apoB) and central obesity do not predict the postprandial PON1 activity and drugs like statins, glitazons and metformin do not affect the postprandial PON1 changes, although some effects on fasting concentrations may be seen. Lifestyle interventions using the Mediterranean diet increase PON1 activity and may thereby decrease the risk fro atherosclerosis

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Alipour, A. et al. (2008). Paraoxonase 1 and Postprandial Lipemia. In: Mackness, B., Mackness, M., Aviram, M., Paragh, G. (eds) The Paraoxonases: Their Role in Disease Development and Xenobiotic Metabolism. Proteins And Cell Regulation, vol 6. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-6561-3_8

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