Brichard S M, Delporte M L, Lambert M
Endocrinology and Metabolism Unit, Saint-Luc University Hospital, University of Louvain, Medical School, Brussels, Belgium.
Horm Metab Res. 2003 Jun;35(6):337-42. doi: 10.1055/s-2003-41353.
Adipose tissue secretes a large number of physiologically active peptides that often share structural properties with cytokines, and are therefore collectively referred to as "adipocytokines". Some of these are almost exclusively secreted by adipose tissue. Leptin, adiponectin and resistin are specific fat-derived hormones that affect fuel homeostasis and insulin action, and may also be involved in hematopoiesis and immune functions. Anorexia nervosa is characterized by chronic self-starvation and severe weight loss, mainly at the expense of adipose tissue. Starvation-induced depletion of fat stores is accompanied by alterations of circulating adipocytokines. Plasma leptin and likely resistin levels are decreased in anorectic patients, while plasma adiponectin levels are increased. These alterations may have potential repercussions in the pathophysiology of anorexia nervosa. Thus, low leptin and high adiponectin may separately or in concert contribute to altered hematopoiesis and immunity, enhanced insulin sensitivity, neuroendocrine disturbances or osteopenia in anorexia nervosa.
脂肪组织分泌大量具有生理活性的肽类物质，这些肽类物质通常与细胞因子具有共同的结构特性，因此被统称为“脂肪细胞因子”。其中一些几乎仅由脂肪组织分泌。瘦素、脂联素和抵抗素是特定的脂肪衍生激素，它们影响能量稳态和胰岛素作用，还可能参与造血和免疫功能。神经性厌食症的特征是慢性自我饥饿和严重体重减轻，主要消耗的是脂肪组织。饥饿导致的脂肪储备消耗伴随着循环脂肪细胞因子的改变。厌食症患者血浆瘦素水平以及可能的抵抗素水平降低，而血浆脂联素水平升高。这些改变可能在神经性厌食症的病理生理学中产生潜在影响。因此，低水平的瘦素和高水平的脂联素可能单独或共同导致神经性厌食症患者的造血和免疫改变、胰岛素敏感性增强、神经内分泌紊乱或骨质减少。
