Dynamic change in adiposity from fetal to postnatal life is involved in the metabolic syndrome associated with reduced fetal growth
Dynamic change in adiposity from fetal to postnatal life is involved in the metabolic syndrome associated with reduced fetal growth
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DOI：
10.1007/s00125-005-1724-4
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发表时间：
2005-05-01
期刊：
影响因子：
8.2
通讯作者：
Lévy-Marchal, C
中科院分区：
文献类型：
--
作者：
Jaquet, D;Deghmoun, S;Lévy-Marchal, C
目的/假设：本研究的目的是确定胰岛素抵抗在与胎儿生长受限相关的代谢综合征中的作用，并阐明胎儿和出生后决定长期代谢结果的因素。研究方法：研究人群包括根据产妇登记处的出生数据选择的成年人，出生时小于胎龄（SGA）（n=734，出生体重<第10百分位数）或适合胎龄（阿加）（n=886，第25 <出生体重<第75百分位数），并在22岁时测量代谢综合征的临床和代谢参数。结果如下：两组间代谢综合征所有组分的平均值均存在显著差异，SGA组中观察到代谢综合征的发生率为2.3%，阿加组为4 ‰（p=0.0004）。在SGA受试者中，空腹胰岛素血症的上三分位数与空腹（p= 0.0001）和OGTT期间（p= 0.0001）的收缩压（p= 0.001）和舒张压（p=0.02）、高胰岛素血症（p = 0.005）和高胰岛素血症的最高值相关。在GA受试者中，胰岛素抵抗与出生体重本身无关（p=0.26），但与出生时的BMI呈负相关（p=0.03），与随后的出生后BMI追赶呈正相关（p=0.009）。结论/解释：胰岛素抵抗是与SGA相关的代谢综合征的关键，其起源应在胎儿发育过程中的肥胖中寻找，该肥胖负责出生后的生长和以后的胰岛素抵抗的发展。
Aims/hypothesis: The aims of this study were to establish the role of insulin resistance in the metabolic syndrome associated with restricted fetal growth and to characterise the fetal and postnatal determinants responsible for the long-term metabolic outcome. Methods: The study population consisted of adults selected on birth data from a maternity registry and born either small for gestational age (SGA) (n=734, birthweight < tenth percentile) or appropriate for gestational age (AGA) (n=886, 25th < birthweight < 75th percentile) and in whom clinical and metabolic parameters of the metabolic syndrome were measured at 22 years of age. Results: Mean values of all components of the metabolic syndrome significantly differed between the two groups, with the metabolic syndrome observed in 2.3% of the SGA group and in 4 parts per thousand of the AGA group (p=0.0004). In SGA subjects, the upper tertile of fasting insulinaemia was associated with the highest values of systolic (p=0.001) and diastolic (p=0.02) blood pressure, triglyceridaemia (p=0.005) and glycaemia at fasting (p=0.0001) and during OGTT (p=0.0001). In GA subjects, insulin resistance was not related to birthweight itself (p=0.26), but correlated negatively with BMI at birth (p=0.03) and positively with the subsequent postnatal catch-up in BMI (p=0.009). Conclusions/interpretation: Insulin resistance is the keystone of metabolic syndrome associated with SGA, and its origin should be sought in the fetal development process of adiposity that is responsible for postnatal growth and the later development of insulin resistance.