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首页> 外文期刊>Psychiatry Research. Neuroimaging >Abnormal relationships between the neural response to high- and low-calorie foods and endogenous acylated ghrelin in women with active and weight-recovered anorexia nervosa
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Abnormal relationships between the neural response to high- and low-calorie foods and endogenous acylated ghrelin in women with active and weight-recovered anorexia nervosa

机译：活动性和体重恢复性神经性厌食症女性对高热量和低热量食物的神经反应与内源性酰化生长素释放肽之间的异常关系

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Evidence contributing to the understanding of neurobiological mechanisms underlying appetite dysregulation in anorexia nervosa draws heavily on separate lines of research into neuroendocrine and neural circuitry functioning. In particular, studies consistently cite elevated ghrelin and abnormal activation patterns in homeostatic (hypothalamus) and hedonic (striatum, amygdala, insula) regions governing appetite. The current preliminary study examined the interaction of these systems, based on research demonstrating associations between circulating ghrelin levels and activity in these regions in healthy individuals. In a cross-sectional design, we studied 13 women with active anorexia nervosa (AN), 9 women weight-recovered from AN (AN-WR), and 12 healthy-weight control women using a food cue functional magnetic resonance imaging paradigm, with assessment of fasting levels of acylated ghrelin. Healthy-weight control women exhibited significant positive associations between fasting acylated ghrelin and activity in the right amygdala, hippocampus, insula, and orbitofrontal cortex in response to high-calorie foods, associations which were absent in the AN and AN-WR groups. Women with AN-WR demonstrated a negative relationship between ghrelin and activity in the left hippocampus in response to high-calorie foods, while women with AN showed a positive association between ghrelin and activity in the right orbitofrontal cortex in response to low-calorie foods. Findings suggest a breakdown in the interaction between ghrelin signaling and neural activity in relation to reward responsivity in AN, a phenomenon that may be further characterized using pharmacogenetic studies.
机译：有助于理解神经性厌食症食欲失调的神经生物学机制的证据在很大程度上依赖于对神经内分泌和神经回路功能的研究。特别是，研究始终引用控制食欲的稳态区（下丘脑）和享乐区（纹状体，杏仁核，岛形）中生长素释放肽的升高和异常激活模式。当前的初步研究基于证明健康个体中这些生长素释放素水平与这些区域活动之间的关联的研究，研究了这些系统的相互作用。在横断面设计中，我们使用食物提示功能磁共振成像范例研究了13例活动性神经性厌食症（AN），9例从AN中恢复体重的妇女（AN-WR）和12例健康体重控制妇女。评估酰化生长素释放肽的禁食水平。体重控制健康的妇女对空腹酰化生长素释放肽与右杏仁核，海马体，岛鞘和眶额皮层活动之间的显着正相关，这是对高热量食物的反应，而在AN和AN-WR组中则没有这种关系。患有AN-WR的女性表现出对高热量食物的反应，生长素释放肽与左海马活动之间呈负相关，而患有AN-WR的女性表现出对低热量食物的反应，生长素释放肽与右眼额叶皮层活动之间呈正相关。研究结果表明，ghrelin信号传导和神经活动之间的相互作用与AN中的奖赏反应性有关，这种现象可能会通过药物遗传学研究进一步表征。

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