Johansen Jeanette E, Fetissov Sergueï O, Bergström Ulrika, Nilsson Ida, Faÿ Charles, Ranscht Barbara, Hökfelt Tomas, Schalling Martin
Karolinska Institutet, Department of Molecular Medicine and Surgery, L8:00, Karolinska University Hospital, S-171 76 Stockholm, Sweden.
Physiol Behav. 2007 Sep 10;92(1-2):278-82. doi: 10.1016/j.physbeh.2007.05.019. Epub 2007 May 21.
Eating disorders constitute major medical health problems in the western world. Even though little is known about the molecular mechanisms behind abnormal eating behavior, it has become clear that the central nervous system (CNS), particularly the hypothalamus, plays a significant role. The anorexic anx/anx mouse is a unique model for studying food intake and energy expenditure. The anx mutation is linked to marked alterations in hypothalamic distributions of signal substances known to have potent regulatory roles in the control of food intake. Another mouse model that displays an anorectic phenotype similar to the anx/anx mouse is the Contactin KO mouse. This model displays very similar hypothalamic alterations as seen in the anx/anx mouse, arguing for a role of these specific hypothalamic changes in an anorectic phenotype. In human eating disorders, hypothalamic systems corresponding to those defective in mouse models could be compromised since autoantibodies against melanocortin peptides have been detected in anorectic and bulimic patients. These findings represent research avenues that may lead to a better understanding of eating disorders and development of targeted therapeutic approaches.
饮食失调是西方世界主要的医学健康问题。尽管对异常饮食行为背后的分子机制知之甚少，但已明确中枢神经系统（CNS），尤其是下丘脑，起着重要作用。厌食的anx/anx小鼠是研究食物摄入和能量消耗的独特模型。anx突变与已知在食物摄入控制中具有强大调节作用的信号物质在下丘脑分布的显著改变有关。另一种表现出与anx/anx小鼠相似厌食表型的小鼠模型是Contactin基因敲除小鼠。该模型显示出与anx/anx小鼠非常相似的下丘脑改变，表明这些特定的下丘脑变化在厌食表型中起作用。在人类饮食失调中，由于在厌食症和贪食症患者中检测到针对黑皮质素肽的自身抗体，与小鼠模型中缺陷相对应的下丘脑系统可能受到损害。这些发现代表了可能有助于更好地理解饮食失调并开发针对性治疗方法的研究途径。
