Does AGE-RAGE Stress Play a Role in the Development of Coronary Artery Disease in Obesity?

This article deals with the role of AGE (advanced glycation end products)-RAGE (receptor for AGE) stress (AGE/sRAGE) in the development of coronary artery disease (CAD) in obesity. CAD is due to atherosclerosis in coronary artery. The serum/plasma levels of AGE and sRAGE are reduced, while AGE-RAGE stress and expression of RAGE are elevated in obese individuals. However, the levels of AGE are elevated in obese individuals with more than one metabolic syndrome. The increases in the AGE-RAGE stress would elevate the expression and production of atherogenic factors, including reactive oxygen species, nuclear factor-kappa B, cytokines, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial leukocyte adhesion molecules, monocyte chemoattractant protein-1, granulocyte-macrophage colony-stimulating factor, and growth factors. Low levels of sRAGE would also increase the atherogenic factors. The increases in the AGE-RAGE stress and decreases in the levels of sRAGE would induce development of atherosclerosis, leading to CAD. The therapeutic regimen for AGE-RAGE stress-induced CAD in obesity would include lowering of AGE intake, prevention of AGE formation, degradation of AGE in vivo, suppression of RAGE expression, blockade of AGE-RAGE interaction, downregulation of sRAGE expression, and use of antioxidants. In conclusion, the data suggest that AGE-RAGE stress is involved in the development of CAD in obesity, and the therapeutic interventions to reduce AGE-RAGE would be helpful in preventing, regressing, and slowing the progression of CAD in obesity.

Flaxseed and Its Components in Treatment of Hyperlipidemia and Cardiovascular Disease.

This paper describes the effects of flaxseed and its components (flax oil, secoisolariciresinoldiglucoside[SDG], flax lignan complex [FLC], and flax fibers] on serum lipids (total cholesterol [TC], low-density lipoprotein-cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides [TG]) in animals and humans. Ordinary flaxseed reduces TG, TC, LDL-C, and TC/HDL-C levels in a dose-dependent manner in animals. In humans, it reduces serum lipids in hypercholesterolemicpatients but has no effects in normocholesterolemicpatients. Flax oil has variable effects on serum lipids in normo- and hypercholesterolemic animals. Flax oil treatment, with a dosage containing greater than 25 g/day of α-linolenic acid, reduces serum lipids in humans. Although FLC reduces serum lipids and raises serum HDL-C in animals, its effects on serum lipids in humans are small and variable. Flax fibers exert small effects on serum lipids in humans. Crop Development Centre (CDC)-flaxseed, which contains low concentrations of α-linolenic acid, has significant lipid lowering effects in animals. Pure SDG has potent hypolipidemic effects and raises HDL-C. In conclusion, flaxseed and pure SDG have significant lipid-lowering effects in animals and humans, while other components of flaxseed have small and variable effects.