Müller Timo D, Föcker Manuel, Holtkamp Kristian, Herpertz-Dahlmann Beate, Hebebrand Johannes
Department of Child and Adolescent Psychiatry and Psychotherapy, University of Duisburg-Essen, Virchowstrasse 174, 45147 Essen, Germany.
Child Adolesc Psychiatr Clin N Am. 2009 Jan;18(1):117-29. doi: 10.1016/j.chc.2008.07.002.
Hypoleptinemia is a key endocrinological feature of anorexia nervosa (AN). Several symptoms in acute AN are related to the low circulating leptin levels including amenorrhea and semi-starvation-induced hyperactivity. The drop in leptin levels results from the loss of fat mass; once leptin levels fall below specific thresholds the hypothalamic-pituitary-gonadal and -thyroid axes are down-regulated; in contrast, the hypothalamic-pituitary-adrenal axis is up-regulated. Hypoleptinemia is the major signal underlying both somatic and behavioral adaptations to starvation. Because the mechanisms involved in this adaptation are similar in rodents and humans, rodent models can be used to investigate the relevant central pathways which underly the respective starvation-induced symptoms. During therapeutically induced weight gain, leptin levels can intermittently increase above normal concentrations. This hyperleptinemia could predispose to renewed weight loss.
低瘦素血症是神经性厌食症（AN）的关键内分泌特征。急性神经性厌食症的几种症状与循环瘦素水平低有关，包括闭经和半饥饿诱导的多动。瘦素水平下降是由于脂肪量减少；一旦瘦素水平降至特定阈值以下，下丘脑 - 垂体 - 性腺轴和下丘脑 - 垂体 - 甲状腺轴就会下调；相反，下丘脑 - 垂体 - 肾上腺轴会上调。低瘦素血症是身体和行为对饥饿适应的主要信号。由于啮齿动物和人类在这种适应过程中涉及的机制相似，因此可以使用啮齿动物模型来研究导致各自饥饿诱导症状的相关中枢途径。在治疗性体重增加期间，瘦素水平可能会间歇性地升高至正常浓度以上。这种高瘦素血症可能会导致体重再次减轻。
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