Whatmore A J, Hall C M, Jones J, Westwood M, Clayton P E
Endocrine Science Research Group, University of Manchester, UK.
Clin Endocrinol (Oxf). 2003 Nov;59(5):649-54. doi: 10.1046/j.1365-2265.2003.01903.x.
In addition to its regulation by GH releasing hormone (GHRH) and somatostatin, release of GH from the pituitary is modulated by a third factor, ghrelin, which is expressed in high concentration in the stomach and is present in the circulation. Ghrelin has also been shown to cause weight gain by increasing food intake and decreasing fat utilization. Ghrelin is a potential candidate hormone to influence nutrient intake and growth. Its role through normal childhood and adolescence has not been fully defined.
Cross-sectional study in 121 healthy children (65 male, 56 female) aged 5-18 years, in whom height, weight, body mass index (BMI), pubertal status and measurements of IGF-I, IGFBP-3, IGFBP-1 and leptin were available.
Serum ghrelin concentrations have been measured in radioimmunoassay (RIA; Phoenix, AZ, USA) that detects active and inactive human ghrelin. Relationships between ghrelin and anthropometric data and growth factors were assessed by correlation and regression analyses.
Ghrelin was detected in all samples, with a median concentration of 162 pg/ml, range 60-493 pg/ml. Prepubertal children had higher ghrelin concentrations than those in puberty [218 pg/ml (n = 42) and 157 pg/ml (n = 79), P < 0.001], with significant negative correlations between ghrelin and age (rs = -0.39, P < 0.001) and pubertal stage (rs = -0.42, P < 0.001). The decrease in ghrelin with advancing pubertal stage/age was more marked in boys than girls. In the whole group, ghrelin was negatively correlated to BMI SD (rs = -0.24, P = 0.006) and to weight SD (rs = -0.24, P = 0.008) but not height sds. Ghrelin was also negatively correlated to IGF-I (rs = -0.48, P < 0.001), IGFBP-3 (rs = -0.32, P < 0.001) and leptin (rs = -0.22, P = 0.02) but not IGF-II. It was positively related to IGFBP-1 (rs = +0.46, P < 0.001). In stepwise multiple regression, 30% of the variability in ghrelin through childhood could be accounted for by log IGF-I (24%) and log IGFBP-1 (6%).
The fall in ghrelin over childhood and with puberty does not suggest that it is a direct growth-promoting hormone. However in view of the negative relationship with IGF-I and the positive relationship with IGFBP-1, this fall in ghrelin could facilitate growth acceleration over puberty.
除了受生长激素释放激素（GHRH）和生长抑素调节外，垂体生长激素（GH）的释放还受到第三种因子——胃饥饿素的调节。胃饥饿素在胃中高浓度表达并存在于循环系统中。胃饥饿素还被证明可通过增加食物摄入量和减少脂肪利用导致体重增加。胃饥饿素是影响营养摄入和生长的潜在候选激素。其在正常儿童期和青春期的作用尚未完全明确。
对121名年龄在5至18岁的健康儿童（65名男性，56名女性）进行横断面研究，这些儿童有身高、体重、体重指数（BMI）、青春期状态以及胰岛素样生长因子-I（IGF-I）、胰岛素样生长因子结合蛋白-3（IGFBP-3）、胰岛素样生长因子结合蛋白-1（IGFBP-1）和瘦素的测量数据。
采用放射免疫分析法（RIA；美国亚利桑那州凤凰城）测定血清胃饥饿素浓度，该方法可检测活性和非活性的人胃饥饿素。通过相关性和回归分析评估胃饥饿素与人体测量数据及生长因子之间的关系。
所有样本均检测到胃饥饿素，中位浓度为162 pg/ml，范围为60 - 493 pg/ml。青春期前儿童的胃饥饿素浓度高于青春期儿童[分别为218 pg/ml（n = 42）和157 pg/ml（n = 79），P < 0.001]，胃饥饿素与年龄（rs = -0.39，P < 0.001）和青春期阶段（rs = -0.42，P < 0.001）呈显著负相关。随着青春期阶段/年龄的增长，胃饥饿素的下降在男孩中比女孩更明显。在整个研究组中，胃饥饿素与BMI标准差（rs = -0.24，P = 0.006）和体重标准差（rs = -0.24，P = 0.008）呈负相关，但与身高标准差无关。胃饥饿素还与IGF-I（rs = -0.48，P < 0.001）、IGFBP-3（rs = -0.32，P < 0.001）和瘦素（rs = -0.22，P = 0.02）呈负相关，但与IGF-II无关。它与IGFBP-1呈正相关（rs = +0.46，P < 0.001）。在逐步多元回归分析中，儿童期胃饥饿素变化的30%可由log IGF-I（24%）和log IGFBP-1（6%）解释。
儿童期及青春期胃饥饿素水平下降并不表明它是一种直接促进生长的激素。然而，鉴于其与IGF-I的负相关关系以及与IGFBP-1的正相关关系，胃饥饿素的这种下降可能有助于青春期的生长加速。
