**1. Introduction**

Non-communicable diseases refer to chronic conditions that are non-infectious and non-transmissible and include obesity, cardiovascular disease, diabetes, cancer, as well as respiratory and neurological diseases. They represent the most common cause of death and disability in developed as well as developing countries [1]. In addition to age-related mitochondrial alterations, oxidative stress and inflammation are key mechanisms in the onset and development of these conditions [2].

Lipids, in particular esterified lipids such as triglycerides (TG), phospholipids, and cholesteryl esters are essential metabolites for energy, cell membrane integrity as well as regulatory hormones. Reactive oxygen species (ROS) are produced by normal physiological processes and play an important role in cell signaling and tissue homeostasis. In view of their high content of polyunsaturated fatty acids (PUFA), lipids transported in plasma lipoproteins as well as those in cellular membranes are especially susceptible to ROS damage, i.e. lipid peroxidation. An imbalance between the formation and detoxification of ROS can lead to the oxidative stress and the nonenzymatic modification of biomolecules, such as proteins, carbohydrates, nucleic acids and lipids. Lipid peroxidation damages surface phospholipids directly and delivery of oxidized fatty acids to the cells play an important role in many inflammatory diseases and can mediate proinflammatory changes [3]. With meal consumption, the intermittent influx of newly absorbed dietary fat in the form of TG-rich chylomicrons is associated with delayed clearance of plasma lipids. This delay is further exacerbated in individuals with metabolic syndrome, type 2 diabetes as well as in obese individuals resulting in greater ROS damage.

Chronic hyperglycemia in diabetes is associated with concomitant increase in the level of ROS and a reduction in enzymatic and nonenzymatic cell antioxidant defenses [4, 5]. In vitro study has demonstrated that intermittent exposure to high glucose environment could stimulate superoxide production and enhance endothelial cell apoptosis to a greater extent than exposure to constant high glucose [6]. In vivo study also noted that intermittent meal-induced elevations in plasma glucose could also play a role in inducing inflammation and oxidative stress [7]. Ingestion of glucose has been reported to result in increased production of tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6) by peripheral blood mononuclear cells, and increased formation of ROS [8, 9]. Furthermore, addition of glucose to a fatty meal delays the metabolism of intestinal chylomicrons in healthy subjects, thus enhancing lipid peroxidation. In fact, there is ample evidence that the impact of postprandial hyperlipidemia and hyperglycemia on inflammation and oxidative stress is independent and cumulative [10].
