**Abstract**

Among the most common non-communicable diseases are obesity, cardiovascular disease, and diabetes, which are responsible for the major cardiometabolic phenotypes. Together with mitochondrial alterations, oxidative stress and inflammation are key molecular mechanisms that contribute to the onset and development of these conditions. Meal consumption is a recurring daily activity that is directly linked to oxidative stress and inflammation. Acute increases in lipids, notably triglycerides, during the postabsorptive period have been suggested to induce a state of inflammation with stimulation of adhesion molecules, cytokines, oxidative stress, and leukocyte activation. Not only lipids but also meal-induced elevations in glucose have also been linked to postprandial oxidative stress and inflammation. The impact of postprandial hypertriglyceridemia and hyperglycemia on oxidative stress and inflammation is not only independent but may be cumulative. It is our hypothesis that, in a system that could not maintain homeostasis to continuous changes of the environment, repeated exposures to meals that provide modest doses of fat and glucose could potentially elicit abnormal responses that contribute to the onset and development of chronic cardiometabolic phenotypes.

**Keywords:** postprandial triglycerides, oxidative stress, inflammation, hypertriglyceridemia, hyperglycemia, cardiometabolic phenotypes
