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

Abstract

Research findings over the past several decades have shown that inflammation is a prominent feature of many chronic diseases, with poor diet being one likely inflammatory stimulus. Specifically, a single high-fat meal (HFM) has been suggested to increase inflammation, although there is currently no consensus with regard to the specific changes in many of the proinflammatory markers that are frequently assessed after an HFM. The aim of this systematic review was to objectively describe the postprandial timing and magnitude of changes in 5 common inflammatory markers: interleukin (IL) 6, C-reactive protein (CRP), tumor necrosis factor (TNF) a, IL-1b, and IL-8. Ten relevant databases were searched, yielding 494 results, of which 47 articles met the pre-established inclusion criteria: 1) healthy men and women aged 18-60 y, 2) consuming a single HFM ($30% fat, $500 kcal), and 3) assessing relevant inflammatory markers postmeal for $2 h. The only marker found to consistently change in the postprandial period was IL-6: on average, from a baseline of ;1.4 pg/mL, it peaked at ;2.9 pg/mL ;6 h post-HFM (an average relative change of ;100%). CRP, TNF-a, IL-1b, and IL-8 did not change significantly in 79% (23 of 29), 68% (19 of 28), 67% (2 of 3), and 75% (3 of 4) of included studies, respectively. We conclude that there is strong evidence that CRP and TNF-a are not responsive at the usual time scale observed in postprandial studies in healthy humans younger than age 60 y. However, future research should further investigate the role of IL-6 in the postprandial period, because it routinely increases even in healthy participants. We assert that the findings of this systematic review on markers of inflammation in the postprandial period will considerably aid in informing future research and advancing clinical knowledge. Adv Nutr 2017;8:213-25.

Raspberries Improve Postprandial Glucose and Acute and Chronic Inflammation in Adults with Type 2 Diabetes

“…In a recently reported systematic review on the magnitude of changes in inflammatory markers in healthy adults, researchers examined 5 most commonly measured inflammatory markers in postprandial studies as follows: CRP, IL-6, -1β, -8, and TNF-α. Among these 5 biomarkers, the review highlights IL-6 to be the most responsive to postprandial meal composition in healthy participants [31]. Our postprandial observations following acute raspberry supplementation conform to these previous findings, and provide further evidence on the meal modulation of cytokines in context of diabetes.…”

Blood cytokine patterns suggest a modest inflammation phenotype in subjects with long‐chain fatty acid oxidation disorders

“…Myocellular concentrations of LCACs as estimated from wet weight vary widely in these dysmetabolic states, but range from >~50 μ mol/L (rodent insulin‐resistant muscle or LCFA‐treated cultured myocytes, Emerson et al. ; Koves et al. ), to >~1 mmol/L (rat or rabbit cardiac ischemia; i.e., Genuth and Hoppel ; Idell‐Wenger et al.…”

Fat food exacerbates post-prandial hypothalamic inflammation involving GFAP+ cells and microglia

“…1B) compared to SD-fed mice. Previous studies have linked HFD consumption to post-prandial systemic inflammation (Cani et al, 2007; Emerson et al, 2017; Ghanim et al, 2009; Herieka and Erridge, 2014; Kelly et al, 2012; Khor et al, 2014). Therefore, we measured the serum levels of the pro-inflammatory cytokines IL-1β, IL-6 and TNFα, pro-inflammatory chemokines CCL2 and CCL5 (Chemokine (C-C motif) Ligand 2-5), as well as endotoxin (lipopolysaccharide, 3OH C14:0) after SD and HFD short-term exposure (1h, 3h and 6h).…”

“…Several studies have shown a link between HFD consumption, inflammation and risk factors associated with obesity. It seems certain that long-term exposure to HFD induces chronic low-grade systemic inflammation, which is responsible for the development of insulin resistance, type 2 diabetes mellitus along with other chronic illnesses such as cardiovascular disease or cancer (Cani et al, 2007; Emerson et al, 2017; Ghanim et al, 2009; Herieka and Erridge, 2014; Kelly et al, 2012; Lumeng and Saltiel, 2011; Thaler and Schwartz, 2010). More recently, hypothalamic inflammation, a process involving neurons, astrocytes and microglia, has been correlated with obesity and chronic HFD consumption (Balland and Cowley, 2017; Baufeld et al, 2016; Buckman et al, 2015; Gao et al, 2014; Guillemot-Legris et al, 2016; Kim et al, 2019; Milanova et al, 2019; Thaler and Schwartz, 2010; Thaler et al, 2012; Valdearcos et al, 2017; Valdearcos et al, 2014), underlining the effect of chronic exposure to HFD on the central inflammatory status.…”

“…Microgliosis has also been found in the ARC after a 72-hour exposure to HFD (Thaler et al, 2012). These findings tempt us and others to speculate that hypothalamic inflammation may not be limited to chronic exposure to dietary fat, but may occur after consumption of a single meal (Cani et al, 2007; Emerson et al, 2017; Ghanim et al, 2009; Herieka and Erridge, 2014; Kelly et al, 2012; Khor et al, 2014). Therefore, we investigated cellular and molecular hypothalamic remodeling in mice that were exposed for the first time to a HFD for short periods of time (1h, 3h or 6h) and we compared it to mice exposed to standard diet (SD).…”