de A Barretto E S, Gill M S, De Freitas M E, Magalhães M M, Souza A H, Aguiar-Oliveira M H, Clayton P E
Department of Endocrinology, Federal University of Sergipe, Rua Claudio Batista, Aracaju, Brazil.
Clin Endocrinol (Oxf). 1999 Nov;51(5):559-64. doi: 10.1046/j.1365-2265.1999.00837.x.
The relationship between GH, body composition and leptin in children remains ill-defined. We have therefore examined the impact of severe GH deficiency (GHD) due to a mutation in the GHRH receptor on serum leptin concentrations and body composition in childhood.
12 affected children and young people (GHD) (4 M:8F, age 5.4-20.1 years, 8 Tanner stage (TS) 1-2, 4 TS 3-5) and 40 healthy controls (C) from the same region (13 M:27F, age 5.3-18.4 years, 20 TS 1-2, 20 TS 3-5).
Percent body fat was determined by infra-red interactance, from which the amounts of fat mass (FM, kg) and fat free mass (FFM, kg) were derived. Serum leptin concentrations were measured in a single fasted, morning serum sample and results expressed as a concentration and as leptin per unit fat mass (L/FM, ng/ml/kg). To control for differences in sex and pubertal maturation, leptin standard deviation scores (leptin SDS) were calculated using normative data from UK children.
FFM was significantly lower in GHD children than in controls (TS 1-2 P < 0.05, TS 3-5 P < 0.001). FM did not differ significantly between the two groups. Serum leptin concentrations, leptin per unit fat mass and leptin SDS were significantly elevated in GHD children both peripubertal and pubertal compared with controls. Using all subjects, stepwise multiple linear regression with FM, FFM, age, puberty and sex as explanatory variables and leptin concentration as the dependent variable indicated that 59% of the variability in leptin could be accounted for by FM (+, 45%), FFM (-, 9%) and sex (+, 5%) (P < 0.001). However on inclusion of GH deficiency (coded GHD = 1, control = 2) as an explanatory variable 73% of the variability in leptin was explained by FM (+, 45%), GHD (-, 22%) and sex (+, 6%) (P < 0.001).
These data indicate that severe GH deficiency in children is associated with elevated leptin concentrations, irrespective of sex or pubertal stage. This increase is not associated with differences in fat mass but is related to reduced fat free mass in GH deficiency. Furthermore in this population there may be an additional effect of GH deficiency on leptin, independent of the influences of sex and body composition.
儿童生长激素（GH）、身体成分与瘦素之间的关系仍不明确。因此，我们研究了因生长激素释放激素（GHRH）受体突变导致的严重生长激素缺乏（GHD）对儿童血清瘦素浓度和身体成分的影响。
12名受影响的儿童和青少年（GHD组）（4名男性：8名女性，年龄5.4 - 20.1岁，8名 Tanner分期（TS）为1 - 2期，4名TS为3 - 5期）以及来自同一地区的40名健康对照者（C组）（13名男性：27名女性，年龄5.3 - 18.4岁，20名TS为1 - 2期，20名TS为3 - 5期）。
通过红外交互作用测定体脂百分比，由此得出脂肪量（FM，kg）和去脂体重（FFM，kg）。在单次空腹的早晨血清样本中测量血清瘦素浓度，结果以浓度以及每单位脂肪量的瘦素（L/FM，ng/ml/kg）表示。为控制性别和青春期成熟度的差异，使用英国儿童的标准数据计算瘦素标准差分数（瘦素SDS）。
GHD儿童的FFM显著低于对照组（TS 1 - 2期P < 0.05，TS 3 - 5期P < 0.001）。两组之间的FM无显著差异。与对照组相比，GHD儿童在青春期前和青春期的血清瘦素浓度、每单位脂肪量的瘦素以及瘦素SDS均显著升高。使用所有受试者，以FM、FFM、年龄、青春期和性别作为解释变量，瘦素浓度作为因变量进行逐步多元线性回归分析表明，瘦素变异性的59%可由FM（ + ，45%）、FFM（ - ，9%）和性别（ + ，5%）解释（P < 0.001）。然而，将生长激素缺乏（编码为GHD = 1，对照 = 2）作为解释变量纳入后，瘦素变异性的73%由FM（ + ）、GHD（ - ）和性别（ + ）解释（P < 0.001）。
这些数据表明，儿童严重生长激素缺乏与瘦素浓度升高相关，与性别或青春期阶段无关。这种升高与脂肪量的差异无关，而是与生长激素缺乏导致的去脂体重减少有关。此外，在该人群中，生长激素缺乏可能对瘦素有额外影响，独立于性别和身体成分的影响。
