Abstract
Children born small for gestational age (SGA) are at increased risk of future glucose intolerance and type 2 diabetes, possibly after due intrauterine metabolic programming. Soluble leptin receptor (SLR) limits leptin access to signal-transducing membrane receptors. The present study examines whether SGA and appropriate for gestational age (AGA) twins differ with regard to their C-peptide, glucose and leptin systems. The markers C-peptide, glucose, fetal leptin, and SLR in cord blood were assessed in children from dichorionic twin pregnancies at delivery. In 32 cases, weight differed by >15% between twins: one demonstrated Intrauterine Growth Retardation (IUGR) (<10th percentile-SGA), while the other did not (AGAI). The other 67 pairs presented appropriate weight for gestational age (AGAII). Placental leptin and placental leptin receptor content were also assessed. Despite the same concentrations of glucose, the SGA twins maintained a higher level of C-peptide [44.48 pmol/l vs. 20.91 pmol/l, p < 0.05] than the AGAI co-twins, higher HOMA index, calculated as [C-peptide] x [Glucose] (p = 0.045), in cord blood, and a higher level of SLR [SGA vs AGAI—mean: 28.63 ng/ml vs. 19.91 ng/ml, p < 0.01], without any differences in total leptin (p = 0.37). However, SGA placentas demonstrated higher leptin level [130.1 pg/100 g total protein vs 83.8 pg/100 g total protein, p = 0.03], without differences in placental leptin receptor (p = 0.66). SGA/IUGR twins demonstrate relative insulin resistance accompanied by decreased fetal and increased placental leptin signaling. We speculate that relative insulin resistance and changes in the leptin system might be the first evidence of processes promoting deleterious metabolic programming for post-natal life.
Highlights
1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; Introduction Since the late 1980’s, it has been known that children born small for gestational age (SGA) have an increased risk of cardiovascular disease in future life[1,2], leading to the formulation of the “developmental origins of health and disease” (DOHaD) hypothesis[3]
The present study examines the glucose homeostasis (C-peptide and glucose) and the leptin system in human fetuses from dichorionic twin pregnancies, where only one twin was affected with Intrauterine growth restriction (IUGR)
The study included 32 dichorionic twin pairs, where one twin had evidence of IUGR (SGA twin), defined as weight difference between twins exceeding 15%, where the weight of the larger twin was adequate for gestational age (AGAI twin)
Summary
Since the late 1980’s, it has been known that children born small for gestational age (SGA) have an increased risk of cardiovascular disease in future life[1,2], leading to the formulation of the “developmental origins of health and disease” (DOHaD) hypothesis[3]. According to DOHaD, an organism exposed to undernourishment in the uterus diverts the restricted nutrients to preserve the growth and function of vital organs, such as brain, at the expense of growth and organs, such as liver and pancreas Though such intrauterine adaptation in conditions of inadequate nutrition is favorable for survival, this has its consequence for the postnatal life through modulation of phenotype; i.e., the so-called “thrifty phenotype hypothesis”[4]. Intrauterine growth restriction (IUGR) is often detected near mid-pregnancy in women and persists until term Both maternal and placental factors are believed to influence IUGR development, with the key maternal risk factors being hypertension, diabetes, metabolic and chronic diseases, smoking, low maternal weight during pregnancy and social economic status[5]. The risk of placental insufficiency is associated with local disturbances in the delivery of oxygen and nutrients into the developing fetus caused by abnormal (shallow) implantation of trophoblast cells into maternal decidua[5]
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