Abstract

ObjectivesExcess fat mass has been associated with poorer cognitive function. Elevated visceral adiposity (VAT) has also been associated with cardiometabolic risk factors including chronic systemic low-grade inflammation. Whereas the cognitive implications of inflammation have been extensively studied in preclinical models, the influence of inflammatory cytokines on human cognition is unclear. Thus, this study aimed to investigate the relations among VAT, inflammatory cytokines and cognitive control. We hypothesized that elevated VAT and inflammation would be related to poorer performance during a cognitive control task. MethodsParticipants between 25–45 years (N = 77 48 females) with overweight/obesity (BMI ≥ 25 kg/m2) underwent a DXA scan to quantify VAT. A Flanker Task was used to assess cognitive control while Event-Related Potentials were recorded. Following an overnight fast, blood was collected to quantify plasma C-reactive protein (CRP) and Interleukin-6 (IL-6) concentrations using ELISAs. Spearman’s correlations were used to analyze relations using a 1-tailed approach. ResultsGreater VAT was related to lower congruent (r = −.19, P = .05) and incongruent trial accuracy (r = −.26, P = .01), as well as lower congruent P3 peak amplitude (r = −.23, P = .02) and slower latency (r = .37, P < .001). Similarly, elevated CRP and IL-6 were associated with poorer congruent (rCRP = −.22 pCRP = .03; rIL6 = −.20 pIL6 = .03), and incongruent (rCRP = −.33 pCRP = .002; rIL6 = −.32 pIL6 = .002) accuracy. Additionally, CRP was related to slower incongruent P3 peak latency (r = .22, P = .02). Partial correlations controlling for CRP and IL-6 showed that VAT was no longer associated with cognitive performance (all p’s > 0.07); however, the association between VAT and P3 peak amplitude (r = −.26, P = .01) and latency (r = .35, P = .001) persisted even following adjustment for CRP and IL-6. ConclusionsThis work replicates previous research indicating that VAT is related to poorer attentional abilities; however, we extend the literature by elucidating the role of low-grade inflammation as a contributing factor in this relationship in adults with excess fat mass. Funding SourcesThis work was supported by funds provided by the Dept of Kinesiology & Community Health at UIUC & the USDA National Institute of Food and Agriculture, Hatch Project 1009249. Partial support provided by the Hass Avocado Board.

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