Opposite changes in circulating adiponectin in women with bulimia nervosa or binge eating disorder
Opposite changes in circulating adiponectin in women with bulimia nervosa or binge eating disorder
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DOI：
10.1210/jc.2003-030956
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发表时间：
2003-11-01
影响因子：
5.8
通讯作者：
Maj, M
中科院分区：
文献类型：
--
作者：
Monteleone, P;Fabrazzo, M;Maj, M
脂联素是最近发现的一种外周肽，仅由分化的脂肪细胞分泌。它已被证明可以增强胰岛素敏感性、控制体重、调节脂质稳态和预防动脉粥样硬化。据报道，神经性贪食症 (BN) 和/或暴食症 (BED) 存在脂质和葡萄糖代谢失调以及体重和体脂肪量变化；因此，脂联素分泌的研究对于这些饮食失调具有明显的意义。为此，我们测量了 60 名未用药女性的血浆脂联素、葡萄糖、胆固醇、甘油三酯和甲状腺激素水平，其中包括 20 名 BN 患者、20 名 BED 患者和 20 名健康对照。与健康女性相比，BN女性的循环脂联素水平（P < 0.002）和胆固醇浓度（P < 0.005）显着升高，而BED女性的血浆脂联素水平显着降低（P < 0.005），葡萄糖（P < 0.01）、胆固醇（P < 0.05）和甘油三酯（P < 0.02）浓度升高。此外，血浆脂联素水平与贪食症患者的暴食/呕吐频率显着相关（r = 0.65，P = 0.002），但与暴食症患者的暴食频率无关。由于我们没有纳入一组不暴饮暴食的肥胖患者，因此应谨慎考虑 BED 研究结果的特异性。然而，根据目前的结果，人们很容易推测，BN 中脂联素产量的增加可能代表了一种抵消可能发生的胰岛素抵抗的补偿机制，而 BED 个体脂联素分泌的减少可能是发生葡萄糖耐受不良的危险因素。
Adiponectin is a recently discovered peripheral peptide that is secreted exclusively by differentiated adipocytes. It has been shown to enhance insulin sensitivity, control body weight, regulate lipid homeostasis, and prevent atherosclerosis. Dysregulation of both lipid and glucose metabolism and changes in body weight and body fat mass have been reported in bulimia nervosa (BN) and/or binge eating disorder (BED); hence, investigation of adiponectin secretion is of obvious interest in these eating disorders. To this purpose, we measured plasma levels of adiponectin, glucose, cholesterol, triglycerides, and thyroid hormones in 60 drug-free women, including 20 patients with BN, 20 patients with BED, and 20 healthy controls. Compared with healthy women, BN women exhibited significantly increased circulating adiponectin levels (P < 0.002) and cholesterol concentrations (P < 0.005), whereas BED women had significantly reduced plasma levels of adiponectin (P < 0.005) and increased concentrations of glucose (P < 0.01), cholesterol (P < 0.05), and triglycerides (P < 0.02). Moreover, plasma levels of adiponectin were significantly correlated to the frequency of binge/vomiting episodes (r = 0.65, P = 0.002) in bulimics but not to the frequency of bingeing in BED patients. Because we did not include a group of obese patients who did not binge eat, the specificity of our findings in the BED should be considered cautiously. However, on the basis of present results, it is tempting to speculate that the increased production of adiponectin in BN may represent a compensatory mechanism to counteract the possible development of insulin resistance, whereas the decreased secretion of adiponectin in individuals with BED may be a risk factor for the development of glucose intolerance.