Weight gain reverses bone turnover and restores circadian variation of bone resorption in anorexic patients
Weight gain reverses bone turnover and restores circadian variation of bone resorption in anorexic patients
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DOI：
10.1046/j.1365-2265.2000.00879.x
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发表时间：
2000-01-01
影响因子：
3.2
通讯作者：
Estour, B
中科院分区：
文献类型：
--
作者：
Caillot-Augusseau, A;Lafage-Proust, MH;Estour, B
目的探讨神经性缺氧（aneroxia nervosa，AN）患者骨重建生化标志物在基线和体重增加后的变化及其昼夜节律。（平均年龄21岁，范围：16-30岁），在研究期间保持闭经，再喂养后体重指数（BMI）较低，以及6名女性对照（平均年龄20岁，范围18-24，BMI：20.6 +/- 1.1 kg/m（2））。再喂养与任何其他干预或治疗无关，特别是雌激素替代或激素避孕。雌二醇的血清水平保持低于70 pmol/L之前和之后refeeding.MEASUREMENTS在研究期间，PTH和25-羟基维生素D的测量进行。骨形成标志物：测定血清完整骨钙素（iBGP）、骨钙素+片段（iBGP+F）和骨吸收指标尿I型胶原C端肽（uCTX）、血清V型胶原C端肽（sCTX）。发现AN患者和对照组之间的骨形成标志物在基线时有显著差异。复饲后，iBGP和iBGP+F水平分别增加了172%和154%，与对照组无差异。正常对照组的完整BGP和iBGP+F具有明显的昼夜节律变化（分别为P < 0.05和P < 0.002），而AN患者则无明显的昼夜节律变化。再喂食后，没有观察到明显的昼夜节律变化;然而，iGBP+F倾向于在清晨达到峰值，下午达到最低点。在基线时，AN患者的sCTX是对照组的2倍。体重增加后sCTX显著下降并达到对照值。再喂养诱导uCTX非显著性降低40%。uCTX与sCTX 24 h平均值呈正相关（r（2）= 0.93，P < 0.0001），uCTX与sCTX 0800 h峰值平均值呈正相关（r（2）= 0.65，P < 0.0003）。对照组血清CTX呈明显的昼夜变化（P < 0.001），峰值出现在0800 h，最低值出现在1600 h，峰值和最低值之间下降60%。我们发现，神经性厌食症抑制sCTX的昼夜变化，恢复再喂养。我们发现AN患者的BMI与sCTX/iBGP比值之间存在显著的非线性关系（r（2）= 0.6，P < 0.0001），从而说明营养状况对骨重塑的影响。结论在这项研究中，我们发现体重增加（仅与再喂养有关）逆转了神经性厌食症引起的骨重塑的解偶联，并恢复了骨吸收标志物的昼夜变化。
OBJECTIVE The present study was conducted in order to describe the variations and circadian rhythm of biochemical markers of bone remodelling at baseline and after weight gain in patients with aneroxia nervosa (AN).SUBJECTS We studied 9 women (mean age 21 years, range: 16-30) with established AN who remained amenorrhoeic during the study and with a low body mass index (BMI) after refeeding and 6 female controls (mean age 20 years, range, 18-24 and BMI: 20.6 +/- 1.1 kg/m(2)). Refeeding was not associated with any other intervention or treatment, especially oestrogen replacement or hormonal contraception. Serum levels of oestradiol remained below 70 pmol/l before and after refeeding.MEASUREMENTS During the study, PTH and 25-hydroxyvitamin D measurements were performed. Markers of bone formation: serum intact osteocalcin (iBGP) and serum intact BGP + fragments (iBGP+F) and markers of bone resorption: urine C-teloptide of type I collagen (uCTX) and serum C-telopeptide ofv-type 1 collagen (s-CTX) were measured.RESULTS At baseline, PTH and 25 OH-vitamin D concentrations were within the normal range in AN patients and no significant variation was observed after refeeding. Bone formation markers were found to be significantly different at baseline between AN patients and controls. After refeeding, iBGP and iBGP+F levels increased by 172% and 154%, respectively, to values no different from controls. Intact BGP and iBGP+F exhibited a significant circadian variation in controls (P < 0.05 and P < 0.002, respectively), whereas we did not find any such circadian rhythm in AN patients. After refeeding no significant circadian variation was observed; however, iGBP+F tended to peak in early morning and exhibited a nadir in the afternoon. At baseline, sCTX was 2-fold higher in AN patients than in controls. After weight gain sCTX decreased significantly and reached control values. Refeeding induced a non-significant 40% decrease in uCTX. We found positive correlations between uCTX and the 24-h mean value of sCTX levels (r(2) = 0.93, P < 0.0001) and between uCTX and the mean value of sCTX peak levels at 0800 h (r(2) = 0.65, P < 0.0003). Serum CTX exhibited a significant circadian variation in controls (P < 0.001) with a peak at 0800 h and a nadir at 1600 h with a 60% decrease between peak and nadir values. We found that anorexia nervosa suppressed the sCTX circadian variation which was restored by refeeding. We found a significant non-linear relationship between BMI and sCTX/iBGP ratio in AN (r(2) = 0.6, P < 0.0001), thus illustrating the influence of nutritional status on bone remodelling.CONCLUSIONS In this study we found that weight gain, related to refeeding only, reversed the anorexia nervosa-induced uncoupling of bone remodelling and restored circadian variation of a bone resorption marker.