High-Fat Meal–Induced Changes in Markers of Inflammation and Angiogenesis in Healthy Adults Who Differ by Age and Physical Activity Level

Abstract

BackgroundInflammation and angiogenesis are key facets of cardiovascular disease pathophysiology. Age and physical activity level can influence fasting systemic inflammation, but the impact of these factors on postprandial inflammation is unknown. In addition, markers of angiogenesis have never been tested in the context of a single high-fat meal (HFM).ObjectiveThe purpose of this study was to investigate the effects of an HFM on markers of inflammation and angiogenesis in individuals of different ages and physical activity levels.MethodsTwenty-two healthy adults—8 younger active (YA) adults (4 men, 4 women; mean ± SD age: 25 ± 5 y), 8 older active (OA) adults (4 men, 4 women; 67 ± 5 y), and 6 older inactive (OI) adults (3 men, 3 women; 68 ± 7 y)—consumed an HFM [63% fat (39% saturated fat, 14% monounsaturated fat, 10% polyunsaturated fat), 34% carbohydrate; 12 kcal/kg body mass; 927 ± 154 kcal]. Fourteen inflammatory and 9 angiogenic markers were measured at baseline and 3 and 6 h postmeal.ResultsSignificant group effects were observed in interleukin (IL)-10 (YA > OA; P = 0.02), IL-23 (YA > OA; P = 0.02), tumor necrosis factor (TNF)-α (OA < OI; P = 0.04), and vascular endothelial growth factor (VEGF)-C (YA < OA; P = 0.001). IL-8, VEGF-A, VEGF-C, and heparin-binding epidermal growth factor–like growth factor significantly increased, whereas granulocyte-macrophage colony-stimulating factor, interferon-γ, IL-1β, IL-5, IL-10, IL-12, IL-13, IL-17A, IL-23, TNF-α, leptin, angiopoietin-2, and follistatin significantly decreased after HFM consumption (P’s < 0.05). Notably, VEGF-A and VEGF-C were significantly higher at 3 h [mean difference: 22.5 pg/mL (VEGF-A); 73.5 pg/mL (VEGF-C)] and 6 h postmeal [mean difference: 26.9 pg/mL (VEGF-A); 81.2 pg/mL (VEGF-C)].ConclusionsA novel finding of this study was the robust increase in VEGF after an HFM. There were also group differences in several inflammatory markers (IL-10 and IL-23 greater in YA than OA, and TNF-α lower in OA than OI) that suggest a potential influence of age and physical activity level.

Effects of a single phosphate-enriched test meal on inflammasome activity and postprandial inflammatory markers in healthy subjects

“…It can be speculated that the rise in plasma IL-6 levels was a metabolic rather than an inflammatory response. A postprandial increase in IL-6 was also found in other studies with healthy subjects [ 27 , 33 , 46 ]. Recent data suggest that IL-6, which is also released during exercise, is necessary to maintain energy homeostasis [ 47 ].…”

Anti-Hyperlipidemia, Hypoglycemic, and Hepatoprotective Impacts of Pearl Millet (Pennisetum glaucum L.) Grains and Their Ethanol Extract on Rats Fed a High-Fat Diet

“…On the other hand, obesity and increased adipose tissue mass are associated with increased inflammatory cytokines and adipokines release. Indeed, obese subjects and animal models have a state of low-grade inflammation and showed higher circulatory levels of different inflammatory cytokines such as TNF-α; IL-6, and CRP [59][60][61]. Also, obesity is associated with impaired adiponectin release from the adipocytes.…”

Fasting, non-fasting and postprandial triglycerides for screening cardiometabolic risk

“…Regardless of the instigating meal, postprandial oxidative stress likely accounts for elevated postprandial oxidised LDL ( 163 , 164 ) , which could enhance foam cell formation. Lastly, the angiogenic factors vascular endothelial growth factor (VEGF)-A and VEGF-C increased in response to a high-fat meal, but implications of this are unclear as VEGF promotes both blood vessel growth and is implicated in plaque expansion and potentially haemorrhage ( 149 , 165 , 166 ) .…”