By Robert H. Eckel
The connection of metabolic ailments to heart problems (CVD) is achieving epidemic proportions. This relates quite often to the expanding occurrence of weight problems, the metabolic syndrome and sort 2 diabetes.This ebook outlines and addresses the metabolic components and comparable illnesses that give a contribution to CVD, together with short introductions to metabolic pathways together with lipid and lipoprotein metabolism, macronutrient gas partitioning, insulin motion and bodyweight rules. Mechanisms that relate to changing into overweight, upkeep of the overweight country, the dyslipidemias, and glucose intolerance/diabetes also are addressed, and the significance of interventions that lessen metabolic threat elements and CVD are coated.
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Extra info for Metabolic Risk for Cardiovascular Disease (American Heart Association Clinical Series)
Example text
Non-high-density lipoprotein cholesterol The combination of VLDL cholesterol and LDL cholesterol, named “non-HDL cholesterol” [2], or perhaps better “atherogenic cholesterol,” is a measurement that generally predicts CVD better than LDL-C, as would be anticipated by its including the two lipoprotein types that promote atherosclerosis and predict CVD [47]. Non-HDL cholesterol is a simple calculation of the difference between total and HDL cholesterol. Since even a large meal raises VLDL-C minimally, non-HDL cholesterol can be used in the non-fasting state, and it is valid in patients with hypertriglyceridemia.
Zheng C, Furtado J, Khoo C, Sacks FM. Apolipoprotein C-III and the metabolic basis for hypertriglyceridemia and the dense LDL phenotype. Circulation 2010;121: 1722–34. 16. Sundaram M, Zhong S, Khalil MB, et al. Expression of apolipoprotein C-III in McARH7777 cells enhances VLDL assembly and secretion under lipid-rich conditions. J Lipid Res 2010;51:150–61. 17. Tarugi P, Averna M, Di Leo E, et al. Molecular diagnosis of hypobetalipoproteinemia: an ENID review. Atherosclerosis 2007;195:e19–327. 18.
ApoC-III is a strong candidate for this mechanism since it inhibits binding of apoE and apoB-100 to hepatic receptors and proteoglycan, and it is present in large amounts on triglyceride-rich VLDL [31]. However, in hypertriglyceridemia, clearance of all apoB lipoproteins is diminished [15], both those with and without apoC-III, suggesting that additional mechanisms must be involved such as reduced activity of lipoprotein lipase, hepatic lipase, or novel receptors such as GPIHBP1 (GPI-anchored HDL-binding protein 1) or proteoglycan [4].