From Fetal Growth Restriction to Adolescent Cardiometabolic Risk: The Impact of Catch-Up Growth and Adiposity.

Birth weight was not independently associated with cardiometabolic risk markers in adolescents.

• Birth weight showed no significant association with adiposity, lipid profile, blood pressure, or glycemic status (p > 0.05 for all outcomes).
• The study included 80 term-born adolescents (40 FGR, 40 controls) matched for age and sex in a cross-sectional design.
• This finding challenges assumptions that fetal size per se is the primary driver of later cardiometabolic risk.

Catch-up growth in the FGR group was significantly correlated with increased BMI and central adiposity.

• Catch-up growth correlated with increased BMI (ρ = 0.680, p < 0.001).
• Catch-up growth correlated with central adiposity measured by waist circumference (ρ = 0.714, p < 0.001).
• These correlations were observed specifically within the FGR group of 40 adolescents.

Catch-up growth in FGR adolescents was significantly correlated with elevated blood pressure.

• Catch-up growth correlated with systolic blood pressure (ρ = 0.448, p = 0.0037).
• Catch-up growth correlated with diastolic blood pressure (ρ = 0.325, p = 0.0409).
• The hypertensive effect of catch-up growth was amplified in overweight/obese adolescents (β = 8.13 mmHg; p = 0.006).

Current BMI largely mediated the associations between catch-up growth and cardiometabolic risk outcomes.

• Mediation analyses showed that current BMI largely explains the associations between catch-up growth and cardiometabolic risk, systolic blood pressure, and waist circumference.
• The estimated effect was β = 2.832 kg/m² per 1-unit increase in ΔZ (p < 0.001).
• This indicates adiposity-mediated pathways are central to the cardiometabolic sequelae of catch-up growth.

Catch-up growth was independently associated with higher leptin levels and a higher leptin/ghrelin ratio.

• Catch-up growth was independently associated with higher leptin levels (β = 220 ng/L; p = 0.022).
• Catch-up growth was independently associated with a higher leptin/ghrelin ratio (β = 2.330; p = 0.034).
• Adipokines assessed included leptin, adiponectin, and ghrelin.
• These findings suggest endocrine pathways, in addition to adiposity-mediated mechanisms, contribute to cardiometabolic susceptibility after FGR.

Fetal growth restriction represents a model of adverse intrauterine programming associated with increased risk of cardiometabolic disorders later in life.

• The study was designed to examine relationships between birth weight, catch-up growth, adipokine signaling, and early cardiometabolic risk in adolescents.
• Anthropometry, blood pressure, lipid profile, fasting glucose, adipokines (leptin, adiponectin), and ghrelin levels were all assessed.
• The study design was cross-sectional with 80 term-born adolescents matched for age and sex.