Abstract # 1783 Metabolic dysfunction, inflammation, and task-induced emotional stress reactivity: Neural and cognitive correlates in 331 middle-aged adults
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- 作者：T. Wolfa ; A. Willettea ; b ; c
- 刊名：Brain, Behavior, and Immunity
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：57
- 期：supp_S
- 页码：e22
- 全文大小：36 K
文摘
Pre-diabetes and type 2 diabetes (T2D) etiology is characterized by insulin resistance (IR) and systemic inflammation. These factors can cause deficits in cognitive and affective processing, particularly psychological stress reactivity. The neural correlates of these deficits are unknown. We wished to determine how T2D, IR, and interleukin-6 (IL-6) were related to psychophysiological, behavioral, and hormonal measures of psychological stress reactivity and negative affect predisposition. Among 331 adults (36–84 years old) from the Midlife in the United States (MIDUS) study, we reviewed startle eye-blink response (EBR) to “unpleasant” versus “pleasant” international affect picture system (IAPS) stimuli. Using resting electroencephalography (EEG), we analyzed right frontal alpha asymmetry, a well-established biomarker of negative affect predisposition. Finally, cognitive performance and cortisol output were gauged during an arithmetic stressor task. Fasting glucose and insulin characterized T2D or the homeostatic model assessment of IR (HOMA-IR). High-sensitivity ELISA was used to derive IL-6. For EBR startle magnitude, higher HOMA-IR strongly corresponded to greater EBR for “unpleasant” versus “pleasant” stimuli [R2 = 0.218, p = .020]. For resting EEG, IL-6 [p = 0.030], or T2D showed greater right frontal alpha asymmetry [p = .011]. During the stressor task, participants with T2D scored 26 ± 2% worse than those with euglycemia [p = .040]. Surprisingly, cortisol output at baseline was lower in participants with T2D and pre-diabetes [p = .025]. These results suggest that dysmetabolism and inflammation may increase stress sensitization both at the neuronal and behavioral level.