Eating behavior in anorexia nervosa - an excess of both orexigenic and anorexigenic signalling?
Eating behavior in anorexia nervosa - an excess of both orexigenic and anorexigenic signalling?
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DOI：
10.1038/sj.mp.4000944
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发表时间：
2001-11-01
影响因子：
11
通讯作者：
Inui, A
中科院分区：
文献类型：
--
作者：
Inui, A
神经性厌食症（AN）是一种以异常饮食行为、体重调节以及对体重和体型的态度和感知障碍为特征的疾病。虽然已经取得了进展，在AN的治疗中，相当一部分患者对治疗的反应有限。多内分泌和！长期饥饿后会发生代谢变化，保存能量和蛋白质。AN患者的许多内分泌发现可能是继发于适应机制。然而，AN与简单饥饿的不同之处在于，过度的摄食刺激（食欲）和摄食抑制（食欲）信号传导是特征性的，产生关于饱腹感和进食欲望的“混合”信号。这导致了由瘦素减少引发的适应性进食反应的失败，瘦素是脂肪组织发出的肥胖信号。以及分别导致食欲和食欲信号传导的增加和减少。摄食调节回路的不平衡移位假说将促食欲皮质激素释放因子和促食欲神经肽Y置于AN的最终共同神经生物学底物中。使用这种受体拮抗剂的治疗性干预可能导致更成功和更有针对性的精神药理学治疗。
Anorexia nervosa (AN) is a disorder characterized by abnormal eating behavior, weight regulation, and disturbances in attitudes and perceptions toward body weight and shape. Although progress has been made, in the treatment of AN, a substantial portion of patients have a limited response to treatment. Multiple endocrine and! metabolic changes occur after prolonged starvation, conserving energy and protein. A number of the endocrine findings in patients with AN may be secondary to adaptive mechanisms. However, AN differs from simple starvation in that excess of both feeding-stimulatory (orexigenic) and feeding-inhibitory (anorexigenic) signalling is characteristic, producing the 'mixed' signal about satiety and desire to feed. This leads to, a failure of the adaptive feeding response that is initiated by a decrease in leptin, an adiposity signal from fat tissue.,, and the resultant increase and decrease of orexigenic and anorexigenic signalling,, respectively. The hypothesis of unbalanced shift of feeding-regulatory circuitry places anorexigenic corticotropin-releasing factor and orexigenic neuropeptide Y in the final common neurobiological substrate for AN. Therapeutic intervention using such receptor antagonists, may lead to more successful and targeted psychopharmacological treatment.