神经性厌食症青春期女孩中肽YY水平升高。

Elevated peptide YY levels in adolescent girls with anorexia nervosa.

作者信息

Misra Madhusmita, Miller Karen K, Tsai Patrika, Gallagher Katie, Lin Alvin, Lee Noel, Herzog David B, Klibanski Anne

机构信息

BUL 457, Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USA.

出版信息

J Clin Endocrinol Metab. 2006 Mar;91(3):1027-33. doi: 10.1210/jc.2005-1878. Epub 2005 Nov 8.

DOI:10.1210/jc.2005-1878

PMID:16278259

Abstract

BACKGROUND

Peptide YY (PYY) is an intestinally derived anorexigen that acts via the Y2 receptor, and Y2 receptor deletion in rodents increases bone formation. Anorexia nervosa (AN) is associated with a deliberate reduction in food intake and low bone density, but endocrine modulators of food intake in AN are not known. In addition, known regulators of bone turnover, such as GH, cortisol, and estrogen, explain only a fraction of the variability in bone turnover marker levels.

HYPOTHESES

We hypothesized that PYY may be elevated in AN compared with controls and may contribute to decreased food intake and bone formation.

METHODS

Fasting PYY was examined in 23 AN girls and 21 healthy adolescents 12-18 yr old. We also examined GH, cortisol, ghrelin, and leptin (overnight frequent sampling) and fasting IGF-I, estradiol, total T3, and bone markers. Macronutrient intake and resting energy expenditure (REE) were measured.

RESULTS

AN girls had higher PYY levels compared with controls (17.8 +/- 10.2 vs. 4.8 +/- 4.3 pg/ml; P < 0.0001). Predictors of log PYY were nutritional markers, including body mass index (r = -0.62; P < 0.0001), fat mass (r = -0.55; P = 0.0003), and REE (r = -0.51; P = 0.0006), and hormones, including GH (r = 0.38; P = 0.004) and T3 (r = -0.59; P = 0.0001). Body mass index, fat mass, REE, GH, and T3 explained 68% of the variability of log PYY. Log PYY predicted percentage of calories from fat (r = -0.56; P = 0.0002) and independently predicted osteocalcin (r = -0.45; P = 0.003), bone-specific alkaline phosphatase (r = -0.46; P = 0.003), N-telopeptide/creatinine (r = -0.55; P = 0.0003), and deoxypyridinoline/creatinine (r = -0.52; P = 0.001) on regression modeling.

CONCLUSION

Elevated PYY may contribute to reduced intake and decreased bone turnover in AN.

摘要

背景

肽YY（PYY）是一种源自肠道的食欲抑制素，通过Y2受体发挥作用，啮齿动物中Y2受体缺失会增加骨形成。神经性厌食症（AN）与刻意减少食物摄入量和低骨密度相关，但AN中食物摄入的内分泌调节因子尚不清楚。此外，已知的骨转换调节因子，如生长激素（GH）、皮质醇和雌激素，只能解释骨转换标志物水平变异性的一小部分。

假设

我们假设与对照组相比，AN患者体内的PYY可能升高，并且可能导致食物摄入量减少和骨形成减少。

方法

检测了23名12 - 18岁AN女孩和21名健康青少年的空腹PYY水平。我们还检测了GH、皮质醇、胃饥饿素和瘦素（夜间频繁采样）以及空腹胰岛素样生长因子-I（IGF-I）、雌二醇、总三碘甲状腺原氨酸（T3）和骨标志物。测量了常量营养素摄入量和静息能量消耗（REE）。

结果

与对照组相比，AN女孩的PYY水平更高（17.8±10.2 vs. 4.8±4.3 pg/ml；P < 0.0001）。PYY对数的预测指标包括营养标志物，如体重指数（r = -0.62；P < 0.0001）、脂肪量（r = -0.55；P = 0.0003）和REE（r = -0.51；P = 0.0006），以及激素，如GH（r = 0.38；P = 0.004）和T3（r = -0.59；P = 0.0001）。体重指数、脂肪量、REE、GH和T3解释了PYY对数变异性的68%。PYY对数可预测脂肪热量百分比（r = -0.56；P = 0.0002），并在回归模型中独立预测骨钙素（r = -0.45；P = 0.003）、骨特异性碱性磷酸酶（r = -0.46；P = 0.003）、N - 端肽/肌酐（r = -0.55；P = 0.0003）和脱氧吡啶啉/肌酐（r = -0.52；P = 0.001）。