Placental leptin: An important new growth factor in intrauterine and neonatal development?
Placental leptin: An important new growth factor in intrauterine and neonatal development?
复制标题
DOI：
10.1542/peds.100.1.e1
复制
发表时间：
1997-07-01
期刊：
影响因子：
8
通讯作者：
Funanage, VL
中科院分区：
文献类型：
--
作者：
Hassink, SG;deLancey, E;Funanage, VL
背景。瘦素是 ob 基因的蛋白质产物，由脂肪细胞产生，似乎在肥胖、饱腹感和活动之间起着联系的作用。还发现瘦素对于小鼠的青春期发育、受孕和怀孕是必需的，并且在青春期前的儿童中增加，与肥胖无关，表明瘦素在儿童生长和发育中发挥作用。这项研究调查了 100 对母亲/新生儿，以确定瘦素在新生儿发育中的作用。检测胎盘组织的瘦素 mRNA，以评估其作为子宫内瘦素产生的来源。方法。一百对母亲/新生儿参加了这项研究。对母体静脉血和新生儿脐带血进行瘦素放射免疫测定。作为对照组，测量了 Tanner 1 期和 2 期 43 名儿童的瘦素浓度。从五名母亲身上获取胎盘组织，并通过逆转录/聚合酶链反应 (RT/PCR) 检测瘦素 mRNA。还测定了人胎盘细胞系 JAR 和 JEG-3 的瘦素 mRNA 表达。结果。所有研究的新生儿中瘦素的平均浓度为 8.8 ng/mL（+/-9.6 标准差）。脐带血中的瘦素浓度与新生儿体重 (r = .51)、体重指数 (BMI) (r = .48) 和手臂脂肪 (r = .42) 相关。瘦素和胰岛素之间没有相关性。当对新生儿和 Tanner 1 期和 2 期儿童的肥胖进行统计共变时，新生儿的瘦素浓度（平均 10.57 ng/mL）高于儿童（平均 3.04 ng/mL）。所有母亲体内瘦素的平均值为 28.8 ng/mL（+/-22.2 标准差）。瘦素浓度与孕前 BMI (r = .56)、分娩时 BMI (r = .74) 和手臂脂肪 (r = .73) 相关。母体瘦素与血清胰岛素相关 (r = .49)。母亲和新生儿瘦素浓度之间没有相关性。百分之十三的新生儿的瘦素浓度比母亲高。来自五个不同胎盘的胎盘组织表达瘦素 mRNA 的水平与脂肪组织相当或更高。两种人滋养层胎盘细胞系 JAR 和 JEG-3 也表达瘦素 mRNA。结论。在儿童和成人中发现的瘦素与肥胖之间的相关性也在新生儿中被发现。在控制肥胖的情况下，与 Tanner 1 期和 2 期儿童相比，新生儿的血清瘦素浓度增加了三倍以上，这表明新生儿的瘦素浓度不能仅用肥胖来解释。母亲瘦素浓度与分娩时的肥胖程度相关，但与新生儿肥胖或瘦素无关。瘦素 mRNA 在胎盘组织和两种人胎盘细胞系中都有表达。这些数据表明瘦素在子宫内和新生儿发育中发挥作用，并且胎盘为生长中的胎儿提供瘦素来源。
Background. Leptin, the protein product of the ob gene, is produced by the adipocyte and seems to function as a link between adiposity, satiety, and activity. Leptin has also been found to be necessary for pubertal development, conception, and pregnancy in mice, and is increased in prepubertal children, independent of adiposity, suggesting a role in childhood growth and development. This study investigated 100 mother/newborn pairs to determine the role of leptin in neonatal development. Placental tissue was assayed for leptin mRNA to evaluate it as a source of leptin production in utero.Methods. One hundred mother/newborn pairs were enrolled in this study. Radioimmunoassay was performed for leptin on maternal venous and newborn cord blood. Leptin concentrations were measured in 43 children in Tanner stages 1 and 2 as a control group. Placental tissue was obtained from five mothers and assayed for leptin mRNA by reverse transcription/polymerase chain reaction (RT/PCR). Human placental cell lines JAR and JEG-3 were also assayed for leptin mRNA expression.Results. Leptin was present in all newborns studied at a mean concentration of 8.8 ng/mL (+/-9.6 standard deviations). Leptin concentrations in cord blood correlated with newborn weight (r = .51), body mass index (BMI) (r = .48), and arm fat (r = .42). There was no correlation between leptin and insulin. When statistically covarying for adiposity for newborns and Tanner stages 1 and 2 children, newborns had greater concentrations of leptin (mean, 10.57 ng/mL) than children (mean, 3.04 ng/mL). Leptin was present in all mothers at a mean value of 28.8 ng/mL (+/-22.2 standard deviations). Leptin concentration correlated with prepregnancy BMI (r = .56), BMI at time of delivery (r = .74), and arm fat (r = .73). Maternal leptin correlated with serum insulin (r = .49). There was no correlation between maternal and newborn leptin concentrations. Thirteen percent of newborns had higher leptin concentrations than their mothers. Placental tissue from five separate placentas expressed leptin mRNA at comparable or greater levels than adipose tissue. Two human trophoblastic placental cell lines, JAR and JEG-3 also expressed leptin mRNA.Conclusions. The correlation between leptin and adiposity found in children and adults was also found in newborns. Serum leptin concentrations in newborns were increased more than three-fold compared with children in Tanner stages 1 and 2 when controlling for adiposity, suggesting that leptin concentrations in the newborn are not explained by adiposity alone. Maternal leptin concentrations correlated with measures of adiposity at delivery but did not correlate with newborn adiposity or leptin. Leptin mRNA was expressed both in placental tissue and in two human placental cell lines. These data suggest that leptin has a role in intrauterine and neonatal development and that the placenta provides a source of leptin for the growing fetus.