Abstract
As inflammatory and oxidative stress are associated with cardiometabolic diseases, detection of abnormal fasting levels of inflammatory and oxidative biomarkers are indicative disease presence and may be too late for any preventive management. Metabolic flexibility refers to the ability of various metabolic processes to compensate for these acute changes and return all metabolites to baseline levels. By monitoring responses of key biomarkers to a standardized physiologic challenge, it is possible to assess the ability of the body to restore homeostasis, that is a measure of metabolic flexibility. Acute changes in lipoprotein-associated biomarkers of oxidative stress have been demonstrated following meal consumption. These include changes in circulating levels of oxidized low-density lipoproteins (LDL), levels of autoantibodies to malondialdehyde-modified LDL, as well as the oxidative susceptibility of isolated plasma LDL. These responses depend on the type and amount of dietary fats in the meal. Management with certain lipid-lowering drugs could also be shown to affect these meal-induced changes. However, plasma levels may be underestimated as we can demonstrate a spike in lipoprotein-associated biomarkers of oxidative stress resulting from the release oxidatively modified epitopes from the arterial wall by an intravenous bolus of heparin.