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Abstract
ObjectiveTo compare the concentrations of adipokines in amniotic fluid (AF) and cord blood collected from discordant dichorionic-diamniotic (DCDA) twin fetuses.Study DesignThe study population included DCDA twins discordant for fetal growth (birth weight difference >10%) who either underwent mid-trimester amniocentesis for routine clinical indication (Cohort 1) or whose amniotic fluid was collected at the time of delivery (Cohort 2). In both cohorts, cord blood was collected at delivery.ResultsA total of 92 twin pairs were enrolled (n = 49 in Cohort 1; n = 43 in Cohort 2). In Cohort 1, the concentrations of adiponectin (median, 68.5 ng/mL vs 61.4 ng/mL; p<0.05) and leptin (median, 13.9 ng/mL vs 11.2 ng/mL; p<0.1) in mid-trimester AF were significantly higher in smaller compared with larger twins. In Cohort 2, the concentration of serpin E1 (median, 246.0 ng/mL vs 182.8 ng/mL; p<0.01) in AF at delivery was significantly higher in smaller twins, but no difference was noted in adiponectin and leptin concentrations. Levels of adiponectin (median, 10425.5 ng/mL vs 11552.0 ng/mL; p<0.005) and leptin (median, 2.1 ng/mL vs 2.6 ng/mL; p<0.005) were significantly lower in the cord blood of smaller twins whereas cord blood concentrations of serpin E1 (median, 15.5 ng/mL vs 13.3 ng/mL; p<0.05) was higher in the smaller twins.ConclusionIn discordant DCDA twin pairs, concentrations of adiponectin, leptin, and serpin E1 in mid-trimester AF, AF at delivery, and cord blood at birth vary significantly but predictably between the smaller and larger twins.
Highlights
The intrauterine environment is known to be a critical determinant of adult health
In Cohort 1, the concentrations of adiponectin and leptin in mid-trimester amniotic fluid (AF) were significantly higher in smaller compared with larger twins
In Cohort 2, the concentration of serpin E1 in AF at delivery was significantly higher in smaller twins, but no difference was noted in adiponectin and leptin concentrations
Summary
The intrauterine environment is known to be a critical determinant of adult health. For example, fetal growth restriction (FGR) is associated with the development of adult metabolic diseases, such as obesity, diabetes, hypertension, and coronary heart disease [1]. In the setting of a suboptimal intrauterine environment, the growth restricted fetus undergoes a series of developmental adaptations including a permanent change in its hypothalamic-pituitary-adrenal axis and in insulin-glucose metabolism. It is these changes that appear to be responsible for the increased risk of metabolic diseases in adulthood [2,3,4]. Fetuses with growth restriction have a reduced overall body fat mass, but a disproportionate increase in visceral fat tissue [7] This central obesity has been associated with rapid catch-up growth and the early development of insulin resistance [6,7,8]
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