High‐fat meal induced postprandial inflammation

Abstract

Raised levels of circulating inflammatory markers are associated with coronary artery disease, obesity and type II diabetes. It has been proposed that the ingestion of high-fat meals may serve as a stimulus to raise systemic inflammatory tone, although interventional studies have yielded conflicting results. We here review 57 studies of high-fat meal induced acute postprandial inflammation to identify the most frequently reported markers of postprandial inflammation and to compare these results with the highly consistent low-grade endotoxaemia model in man. Most plasma borne markers of inflammation, such as cytokines and soluble adhesion molecules, were not consistently raised after a high-fat meal. However, pro-inflammatory leukocyte surface markers, mRNA and proteins were elevated in almost all studies in which they were measured. These markers followed kinetics similar to those observed following intravenous injection of low doses of endotoxin in man, were positively associated with likelihood of contamination of test meals with pro-inflammatory bacterial molecules and were reduced in several studies examining parallel meals supplemented with foodstuffs containing anti-inflammatory phytochemicals. Future studies of postprandial inflammation may yield more consistent evidence by focusing on leukocyte, rather than plasma-borne, markers of inflammation and by considering the test meal content of pro- and anti-inflammatory dietary constituents.

Magnitude and Timing of the Postprandial Inflammatory Response to a High-Fat Meal in Healthy Adults: A Systematic Review

“…The present review found that the majority of studies detected an increase in IL-6 after the consumption of an HFM, which agrees with the findings of Herieka and Erridge (12). The increase is generally robust, because the average relative increase is ;100% of the baseline value; thus, IL-6 is quite FIGURE 3 Correlations of several study variables with percentage change in IL-6 from pre-to post-HFM in healthy participants.…”

“…Specifically, TNF-a, like IL-6, is believed to increase quickly in the poststimulus period, peaking at ;2-3 h, then returning quickly to baseline (12). However, the findings of the current review disagree with this notion in the context of an HFM.…”

“…There is also evidence that proinflammatory cytokines, such as IL-6 and TNF-a, directly increase insulin resistance in adipocytes (59). Finally, locally produced proinflammatory cytokines often travel to the liver and increase the production of acute-phase response proteins, such as CRP and serum amyloid A (SAA) (6,12). CRP and SAA are strongly associated with chronic disease risk.…”

“…Instead, CRP will slowly increase and peak at ;24 h poststimulus. [Note: these responses are typically experimentally described by using an endotoxin model, not necessarily an HFM (12).] Thus, because CRP and other acute-phase response proteins reflect the cumulative inflammatory response (i.e., include the amplification and stimulation of many locally produced inflammatory molecules and their subsequent stimulation of acute-phase response proteins in the liver), as well as bearing in mind the delayed increase and decrease in acute-response phase proteins, CRP is a particularly advantageous marker of chronic inflammation to assess both clinically and in research.…”

“…Indeed, when rodents are fed a high-fat diet, there is an increase in markers of inflammation both in adipose tissue and in the systemic vasculature (9)(10)(11). Thus, a diet high in fat and overall energy may partly cause the elevated systemic inflammation that underpins CVD, as well as insulin resistance, and is associated with obesity (12). However, the effect of dietary consumption on inflammation may not be limited to chronic intake but may be evident after the consumption of a single meal.…”