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Published on: February 2, 2017
From Fetal Growth Restriction to Adolescent Cardiometabolic Risk: The Impact of Catch-Up Growth and Adiposity
Anca Adam-Raileanu1, Alin Horatiu Nedelcu1, Mitica Ciorpac1
1Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, Romania.
Insights
Postnatal growth acceleration, not just fetal size, increases cardiometabolic risk in adolescents born with fetal growth restriction (FGR). This catch-up growth impacts BMI, blood pressure, and adipokine signaling, highlighting key pathways for intervention.
Area of Science:
- Endocrinology
- Pediatric Cardiology
- Developmental Biology
Background:
- Fetal growth restriction (FGR) is linked to later-life cardiometabolic disorders.
- Understanding the impact of intrauterine programming on adolescent health is crucial.
Purpose of the Study:
- To investigate the relationship between birth weight, postnatal catch-up growth, adipokine signaling, and early cardiometabolic risk in adolescents.
- To identify the mechanisms linking FGR to adolescent cardiometabolic outcomes.
Main Methods:
- Cross-sectional study of 80 adolescents (40 FGR, 40 controls) matched for age and sex.
- Assessment of anthropometry, blood pressure, lipid profile, glucose, and adipokines (leptin, adiponectin, ghrelin).
- Analysis of associations between birth weight, growth rate, adipokines, and cardiometabolic markers.
Main Results:
- Birth weight was not associated with cardiometabolic risk factors.
- Catch-up growth in FGR adolescents correlated with increased BMI, central adiposity, and blood pressure.
- BMI mediated the link between catch-up growth and cardiometabolic risk; this effect was amplified in overweight/obese adolescents.
- Catch-up growth was linked to higher leptin levels and leptin/ghrelin ratio.
Conclusions:
- Postnatal growth acceleration, not fetal size, is the primary driver of early cardiometabolic risk after FGR.
- Adiposity-mediated and endocrine pathways, involving adipokines, are key mechanisms.
- Targeting postnatal growth and adiposity may mitigate long-term cardiometabolic consequences of FGR.
Abstract:
Background/Objectives: Fetal growth restriction (FGR) represents a model of adverse intrauterine programming associated with an increased risk of cardiometabolic disorders later in life. We examined the relationships between birth weight, catch-up growth, adipokine signaling, and early cardiometabolic risk in adolescents. Methods: This cross-sectional study included 80 term-born adolescents (40 FGR, 40 controls) matched for age and sex. Anthropometry, blood pressure, lipid profile, fasting glucose, adipokines (leptin, adiponectin), and ghrelin levels were assessed. Associations between birth weight, growth rate, adipokines, and cardiometabolic outcomes were analyzed. Results: Birth weight was not associated with adiposity, lipid profile, blood pressure, or glycemic status (p > 0.05). In contrast, catch-up growth in the FGR group was correlated with increased BMI (ρ = 0.680, p < 0.001), central adiposity (ρ = 0.714, p < 0.001), systolic blood pressure (ρ = 0.448, p = 0.0037) and diastolic blood pressure (ρ = 0.325, p = 0.0409). Mediation analyses showed that the current BMI largely explains the associations between catch-up growth and cardiometabolic risk, systolic blood pressure, and waist circumference (β = 2.832 kg/m2 per 1-unit increase in ΔZ; p < 0.001). The hypertensive effect of catch-up growth was amplified in overweight/obese adolescents (β = 8.13 mmHg; p = 0.006). Catch-up growth was independently associated with higher leptin (β = 220 ng/L; p = 0.022) and a higher leptin/ghrelin ratio (β = 2.330; p = 0.034). Conclusions: Postnatal growth acceleration, rather than fetal size alone, drives early cardiometabolic susceptibility following FGR through adiposity-mediated and endocrine pathways.
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