Bosy-Westphal Anja, Brabant Georg, Haas Verena, Onur Simone, Paul Thomas, Nutzinger Detlef, Klein Harald, Hauer Maren, Müller Manfred J
Institut für Humanernährung und Lebensmittelkunde, Agrar- und Ernährungswissenschaftliche Fakultät, Christian-Albrechts-Universität zu Kiel, Düsternbrooker Weg 17-19, 24105, Kiel, Germany.
Eur J Nutr. 2005 Sep;44(6):355-9. doi: 10.1007/s00394-005-0533-3. Epub 2005 Apr 4.
To examine the determinants of adiponectin levels (i) in 23 women with anorexia nervosa (mean BMI 15.0 +/- 1.2) and 43 healthy normal weight females (mean BMI 22.3 +/- 2.3; cross-sectional design) as well as (ii) after six and twelve weeks of weight gain in subgroups of 18 and 11 anorectic patients (mean weight gain 5.8 kg; longitudinal design). Plasma adiponectin and leptin concentrations were measured and their relationships to body composition (fat mass by bioelectrical impedance analysis and anthropometrics), different hormones and metabolic parameters (insulin, ACTH, cortisol, glucose, FFA, lipid profile) were investigated.
In anorectic patients, adiponectin levels were higher (+29 %) and leptin levels were lower (-75 %) than in control subjects. There was a high variance in adiponectin levels in patients ranging from 2.6 to 18 nM. Combining patients and controls, an inverse linear correlation was observed between adiponectin levels and fat mass (r = -0.36, p < 0.05), while a positive exponential relation was found between leptin levels and fat mass (r = 0.82, p < 0.001). In anorectic patients, there were no significant correlations between adiponectin and hormonal or metabolic parameters. Weight gain resulted in increasing leptin (+0.17 +/- 0.12 nM; p < 0.001) and a nonsignificant decrease in adiponectin concentrations (-1.12 +/- 2.51 nM). Changes in leptin levels were mainly explained by a gain in fat mass (r = 0.85, p < 0.001). In contrast, changes in adiponectin levels were closely linked to initial adiponectin levels (r = -0.84, p < 0.001) but not to changes in fat mass or BMI.
Cross-sectionally serum adiponectin concentration followed a linear inverse function with fat mass when patients and controls were combined. Longitudinally gain in fat mass was not associated with changes in adiponectin levels suggesting other yet unidentified influences on adiponectin secretion in anorexia nervosa.
（i）在23名神经性厌食症女性患者（平均体重指数15.0±1.2）和43名健康正常体重女性（平均体重指数22.3±2.3；横断面设计）中，研究脂联素水平的决定因素；以及（ii）在18名和11名神经性厌食症患者亚组体重增加6周和12周后（平均体重增加5.8kg；纵向设计），研究脂联素水平的决定因素。测量血浆脂联素和瘦素浓度，并研究它们与身体组成（通过生物电阻抗分析和人体测量学测定的脂肪量）、不同激素和代谢参数（胰岛素、促肾上腺皮质激素、皮质醇、葡萄糖、游离脂肪酸、血脂谱）之间的关系。
与对照组相比，神经性厌食症患者的脂联素水平较高（+29%），而瘦素水平较低（-75%）。患者的脂联素水平差异很大，范围在2.6至18nM之间。将患者和对照组合并后，观察到脂联素水平与脂肪量呈负线性相关（r = -0.36，p < 0.05），而瘦素水平与脂肪量呈正指数关系（r = 0.82，p < 0.001）。在神经性厌食症患者中，脂联素与激素或代谢参数之间无显著相关性。体重增加导致瘦素水平升高（+0.17±0.12nM；p < 0.001），脂联素浓度无显著下降（-1.12±2.51nM）。瘦素水平的变化主要由脂肪量增加所解释（r = 0.85，p < 0.001）。相比之下，脂联素水平的变化与初始脂联素水平密切相关（r = -0.84，p < 0.001），但与脂肪量或体重指数的变化无关。
横断面研究中，当将患者和对照组合并时，血清脂联素浓度与脂肪量呈线性反比关系。纵向研究中，脂肪量增加与脂联素水平变化无关，这表明在神经性厌食症中，脂联素分泌还受其他尚未明确的影响因素。
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