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神经性厌食症患者及患有运动性厌食症的优秀体操运动员的低瘦素血症。

Hypoleptinaemia in patients with anorexia nervosa and in elite gymnasts with anorexia athletica.

作者信息

Matejek N, Weimann E, Witzel C, Mölenkamp G, Schwidergall S, Böhles H

机构信息

Johann Wolfgang Goethe-University, Centre for Child Health, Clinic for Paediatric Endocrinology and Metabolism, Frankfurt/Main, Germany.

出版信息

Int J Sports Med. 1999 Oct;20(7):451-6. doi: 10.1055/s-1999-8834.

Abstract

Leptin, the product of the ob-gene, is specifically released by adipocytes. In addition to its metabolic function it seems to affect the feedback-mechanisms of the hypothalamic-pituitary-gonadal-axis. We studied 13 female juvenile elite gymnasts with anorexia athletica (AA) and 9 female patients with anorexia nervosa (AN) regarding the relation between leptin, fat stores, and the reproductive hormone levels. Leptin levels in females with anorexia nervosa (Tanner stage B4 [median]; mean age: 17.8 +/- 1.7 years) were low (2.9 +/- 2.7 microg/L), and were related to body mass index (BMI) (r = 0.71; p = 0.03) and percentage body fat mass (r = 0.78; p = 0.01). Leptin levels of the elite gymnasts were even more decreased (1.2 +/- 0.8 microg/L) caused by the low amount of fat stores. Leptin correlated with BMI (r= 0.77; p = 0.004) and the percentage body fat mass (r = 0.6; p = 0.04). In elite gymnasts leptin levels correlated with CA showing an age-dependent increase (r= 0.59; p = 0.04). Oestradiol was secreted at a low level in both groups (AN: 25.6 +/- 17.4 microg/L; AA: 24.4 +/- 13.5 microg/L). A delay in menarche and a retarded bone maturation occurred in AA. Our results clearly show that leptin levels are low in restrained eaters. Leptin levels represent the fat stores in the body and play a permissive role for female pubertal development. There is evidence that the mechanisms leading to a dysregulation of the reproductive-axis in patients with AN are comparable with those leading to delayed puberty in juvenile elite gymnasts with AA. This implies that AN and AA are overlapping groups and AA can lead to the development of AN.

摘要

瘦素是ob基因的产物,由脂肪细胞特异性释放。除了其代谢功能外,它似乎还会影响下丘脑 - 垂体 - 性腺轴的反馈机制。我们研究了13名患有运动性厌食(AA)的女性青少年精英体操运动员和9名神经性厌食(AN)女性患者的瘦素、脂肪储备与生殖激素水平之间的关系。神经性厌食女性(坦纳分期B4[中位数];平均年龄:17.8±1.7岁)的瘦素水平较低(2.9±2.7μg/L),且与体重指数(BMI)相关(r = 0.71;p = 0.03)以及体脂百分比相关(r = 0.78;p = 0.01)。由于脂肪储备量低,精英体操运动员的瘦素水平甚至更低(1.2±0.8μg/L)。瘦素与BMI相关(r = 0.77;p = 0.004)以及与体脂百分比相关(r = 0.6;p = 0.04)。在精英体操运动员中,瘦素水平与骨龄相关,呈现出随年龄增长的趋势(r = 0.59;p = 0.04)。两组的雌二醇分泌水平都较低(AN组:25.6±17.4μg/L;AA组:24.4±13.5μg/L)。运动性厌食患者出现月经初潮延迟和骨成熟迟缓。我们的结果清楚地表明,饮食受限者的瘦素水平较低。瘦素水平代表体内的脂肪储备,对女性青春期发育起允许作用。有证据表明,导致神经性厌食患者生殖轴失调的机制与导致患有运动性厌食的青少年精英体操运动员青春期延迟的机制类似。这意味着神经性厌食和运动性厌食是重叠的群体,运动性厌食可能会导致神经性厌食的发生。

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