Tumor necrosis factor-α:: is there a continuum of liability between stress, anxiety states and anorexia nervosa?
Tumor necrosis factor-α:: is there a continuum of liability between stress, anxiety states and anorexia nervosa?
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DOI：
10.1054/mehy.1997.0641
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发表时间：
1999-02-01
影响因子：
4.7
通讯作者：
Pakula, IS
中科院分区：
文献类型：
--
作者：
Holden, RJ;Pakula, IS
自弗洛伊德时代以来，精神病学就接受了这样的观点：生理和/或心理压力会导致各种精神疾病。为此，我们提出在压力、焦虑状态和神经性厌食症之间存在责任的连续体——这一连续体基于每种情况所共有的细胞因子谱。例如，对压力、焦虑状态和神经性厌食症的生物反应包括白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）的升高，以及干扰素-γ（IFN-γ）的下调。 IL-1β 和 TNF-α 的持续升高会导致生长抑素和胰岛素分泌失调，从而影响局部脑血流量 (rCBF) 和脑能量代谢。此外，IL-1β和TNF-α影响某些关键神经肽的表达，这些神经肽已知与焦虑状态和神经性厌食症有关。这些神经肽包括：β-内啡肽、胆囊收缩素（CCK）、神经肽Y（NPY）和血管活性肠肽（VIP）。 β-内啡肽影响边缘系统中的葡萄糖代谢，CCK 增加垂体前叶释放 β-内啡肽，NPY 是一种强大的抗焦虑药，可调节 β-内啡肽和胰岛素，而 VIP 通过抑制白介素-4 (IL-4) 间接调节 TNF-α 的表达。
Since the time of Freud, psychiatry has embraced the proposition that physiological and/or psychological stress precipitates various psychiatric disorders. To this effect, we propose that a continuum of liability obtains between stress, anxiety states and anorexia nervosa - a continuum which is grounded on a cytokine profile common to each of these conditions. For example, the biological response to stress, anxiety states and anorexia nervosa includes the elevation of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), and downregulation of interferon-gamma (IFN-gamma). Sustained elevation of IL-1 beta and TNF-alpha dysregulates both somatostatin and insulin secretion, the tatter of which influences regional cerebral blood flow (rCBF) and brain energy metabolism. In addition, IL-1 beta and TNF-alpha influence the expression of certain crucial neuropeptides, which are known to be associated with anxiety states and anorexia nervosa. These neuropeptides include: beta-endorphin, cholecystokinin (CCK), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). beta-endorphin effects glucose metabolism in the limbic system, CCK increases the release of beta-endorphin from the anterior pituitary, NPY is a powerful anxiolytic that regulates beta-endorphin and insulin, while VIP indirectly regulates the expression of TNF-alpha through the inhibition of interleukin-4 (IL-4).