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1) (Marzano et al
Clinical Consultations: The time spent with your provider to manage your dosage and side effects
Archived from the original on 2018-02-28
You take the drug, your stomach slows down
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Moreover, the number of LDL-C B/E receptors on the cell surface is considerably diminished,[] which may be due to a decrease in the expression of insulin and can lead to disruption of LDL-C catabolism.[ , ] Changing LDL-C compositions may cause conformational changes and probably results in higher exposure of fatty acids to oxygen-free radicals and changes in lipid peroxidation levels.[ , ] In plasma or subendothelial arterial wall, uptake of LDL-C will increase via scavenger receptors present in macrophages, smooth muscle cells, and endothelial cells as consequences of LDL-C oxidation.[ , , , ] The formation of foam cells as well as the alteration of monocytes and macrophages in the arterial wall to cholesterol foam cells, which are essential parts of the atherosclerosis plaque, significantly increases with the oxidative changes in LDL-C.[ , ] Moreover, in individuals with diabetes, levels of serum lipids are often elevated and are independently related to some complications of DM.[ , ] Higher levels of insulin in the blood, the presence of non-oxidative glycation products, and increases in levels of blood glucose[] because of insulin resistance may increase the risk of cardiovascular morbidity in type 2 diabetes.[] The risk of oxidative stress, which has a vital role in LDL-C oxidation and hyperglycemia, is high in individuals with diabetes.[ , ] Many pharmacological agents, such as calcium channel antagonists and antiplatelet[] agents, have been used in the treatment of peripheral arterial disease (PAD) in individuals with diabetes
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