Postprandial Inflammation: Targeting Glucose and Lipids

Abstract

Many risk factors have been identified as being responsible for the process of atherogenesis. Several of these risk factors are related to inflammation, which is an obligatory feature of the atherosclerotic plaque. Increasing evidence suggests that postprandial lipoproteins and glucose may be involved in the inflammatory process preceding the development of atherosclerosis. During the postprandial situation, remnants of chylomicrons and very low-density lipoproteins bind to circulating leukocytes and endothelial cells, leading to a state of acute activation with the expression of integrins on different cells, the generation of oxidative stress, production of cytokines and complement activation. Elevated plasma glucose levels may also induce leukocyte activation in humans. In addition, advanced glycation end products, formed during hyperglycemia, cause inflammation and endothelial damage. This chain of events results in a situation of acute inflammation causing endothelial dysfunction, which may be one of the earliest defects in atherogenesis. Interestingly, while this may occur several times each day after each meal, there is only limited information on the contribution of different nutrients on the postprandial inflammatory processes. In this review, we will focus on the available evidence and we will discuss the role of lifestyle and pharmaceutical interventions in modulating postprandial inflammation.

Comparisons of the Postprandial Inflammatory and Endotoxaemic Responses to Mixed Meals in Young and Older Individuals: A Randomised Trial

“…Inflammatory gene expression [16], plasma cytokines [18], and endotoxaemia [25] are reported to be particularly elevated after high-fat or high-caloric meals [55] in metabolically-compromised adults, such as those with T2DM and metabolic syndrome. These acute meal responses may contribute to a state of chronic low-grade inflammation, accelerating the development of insulin resistance and cardiovascular disease through progression of atherosclerosis [56,57]. To our surprise, no marked difference in postprandial endotoxaemia or inflammation was seen between younger and older subjects in the current study, suggesting that older adults do not display a greater acute inflammatory response to ingestion of a single high-fat meal.…”

Impairment of lysophospholipid metabolism in obesity: altered plasma profile and desensitization to the modulatory properties of n–3 polyunsaturated fatty acids in a randomized controlled trial

“…In contrast, long-term intake of corn oil, rich in the n-6 PUFA linoleic acid (18:2n-6), had no effects on the response of saturated lysophosphatidylcholines to the HFM challenge, although the concentration of lysophosphatidylcholine 20:4 was increased. It is believed that the postprandial state is a period of transient acute inflammation that contributes to increasing cardiovascular disease risk (40). Therefore, it could be hypothesized that, together with other mechanisms (19,38), n-3 PUFAs might attenuate postprandial inflammation by modulating the metabolism of lysophospholipids.…”

Meal rich in carbohydrate, but not protein or fat, reveals adverse immunometabolic responses associated with obesity

“…Furthermore, advanced glycation end products (AGEs) are formed, taken up by the aforementioned cells and results in activation of mitogen-activated protein kinase (MAPK) pathway and subsequently NF-κB pathway. This finally culminates in production of cytokines, complement activation and generation of oxidative stress [12–14]. …”

“…Further, HC meal induces a more prominent and prolonged postprandial oxidative stress and inflammatory response in MNC in obese individuals in comparison to lean individuals [11]. The higher glucose excursion may contribute to such unabated and excessive inflammatory response by acute activation of inflammatory pathways as well as generation of oxidative stress in circulating MNC, macrophages, smooth muscle cells and endothelial cells [12–14]. Such perturbation in regulation of postprandial inflammatory responses, suggested as one of the earliest defects in atherogenesis, may contribute to obese individuals having a higher risk for cardiovascular diseases [14, 15].…”