By Robert H. Eckel
The connection of metabolic ailments to heart problems (CVD) is attaining epidemic proportions. This relates regularly to the expanding occurrence of weight problems, the metabolic syndrome and sort 2 diabetes.This e-book outlines and addresses the metabolic elements and similar 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 legislation. Mechanisms that relate to turning into overweight, upkeep of the overweight kingdom, the dyslipidemias, and glucose intolerance/diabetes also are addressed, and the significance of interventions that decrease metabolic threat components and CVD are lined.
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Additional info for Metabolic Risk for Cardiovascular Disease (American Heart Association Clinical Series)
Sample text
Atherosclerosis 2007;191:391–6. 45. Juurinen L, Tiikkainen M, Hakkinen AM, et al. Effects of insulin therapy on liver fat content and hepatic insulin sensitivity in patients with type 2 diabetes. Am J Physiol Endocrinol Metab 2007;292:E829–35. 46. Kelley DE, Goodpaster BH, Storlien L. Muscle triglyceride and insulin resistance. Annu Rev Nutr 2002;22:325–46. 47. Goodpaster BH, He J, Watkins S, Kelley DE. Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes.
In some studies people who have insulin resistance or type 2 diabetes have a delayed return of postprandial TG-rich lipoprotein levels to fasting baseline [12]. However, it has not been proven that these lipoproteins that stay in plasma are more atherogenic than those in the fasting state in the same people. A meta-analysis showed that non-fasting and fasting TG predicted CVD similarly [8]. However, in most of the component studies, nonfasting TG was measured at random rather than at a specified interval after a specified meal.
Apolipoprotein C-III exists in HDL and may reduce its protective action to inhibit adhesion of monocytes to endothelial P1: SFK/UKS c02 P2: SFK BLBK331-Eckel Color: 4C August 25, 2010 16:8 Trim: 9in X 6in Chapter 2 Lipid and lipoprotein metabolism 35 cells [34]. ApoC-III in HDL is not a protective marker for CHD, unlike ApoA-I, its principal protein; in fact, HDL apoC-III is associated with increased CHD [72,73]. Clinical application: causes of low high-density lipoprotein cholesterol Low HDL concentrations, measured either by its cholesterol or ApoA-I concentration, are associated with many of the same conditions that cause high TG, overweight, insulin resistance, type 2 diabetes, sedentary habits, and high carbohydrate diets.
