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Published on: June 29, 2013
Both intrauterine growth restriction and postnatal growth influence childhood serum concentrations of adiponectin
Abel López-Bermejo1, Paula Casano-Sancho, José Manuel Fernández-Real
1Diabetes, Endocrinology and Nutrition Unit, Dr Josep Trueta Hospital of Girona, Girona, Spain. uden.alopez@htrueta.scs.es
Insights
Children born small for gestational age (SGA) exhibit higher insulin resistance and adiponectin levels, unless they become overweight. These findings highlight the complex relationship between birth size, metabolic health, and adiponectin in SGA individuals.
Area of Science:
- Pediatric Endocrinology
- Metabolic Health
- Growth and Development
Background:
- Intrauterine growth restriction is linked to insulin resistance.
- Adiponectin is a key regulator of insulin sensitivity.
- Understanding adiponectin's role in SGA children is crucial for metabolic health.
Purpose of the Study:
- To investigate the relationship between birth weight, insulin sensitivity, and circulating adiponectin levels in children born small for gestational age (SGA).
- To determine how insulin resistance and SGA status influence adiponectin concentrations.
- To explore the impact of overweight on adiponectin levels in SGA children.
Main Methods:
- A cross-sectional study involving 32 prepubertal children born SGA and 37 born appropriate for gestational age (AGA).
- Assessment of fasting glucose, lipids, insulin, and adiponectin levels.
- Calculation of insulin resistance (IR) and beta-cell function using the Homeostasis Model Assessment (HOMA).
Main Results:
- SGA children older than 3 years showed higher insulin resistance (HOMA-IR) compared to AGA children.
- Circulating adiponectin concentrations were significantly higher in SGA children.
- Overweight SGA children had lower adiponectin levels compared to lean SGA children.
- Insulin resistance and SGA status explained 35% and 15% of adiponectin variance, respectively.
Conclusions:
- Prenatal growth restriction is associated with insulin resistance and elevated adiponectin, provided overweight is absent.
- The role of adiponectin in the increased risk of insulin resistance and type-2 diabetes in former SGA subjects requires further investigation.
- Early metabolic monitoring in SGA children is essential to mitigate long-term health risks.
Objective:
Insulin resistance has been linked to intrauterine growth restriction; adiponectin is a strong determinant of insulin sensitivity. We aimed at studying the contributions of birthweight and insulin sensitivity to circulating adiponectin in children born small for gestational age (SGA).
Design:
Cross-sectional, hospital-based study dealing with insulin sensitivity in SGA children.
Patients:
Thirty-two prepubertal children born SGA (age 5.4 +/- 2.9 years) and 37 prepubertal children born appropriate for gestational age (AGA, age 5.9 +/- 3.0 years).
Measurements:
Serum levels of fasting glucose, serum lipids, insulin (immunometric assay) and adiponectin concentrations (ELISA) were assessed, and insulin resistance (IR) and insulin secretion (beta-cell) were calculated by the homeostasis model of assessment (HOMA).
Results:
SGA children had similar HOMA-IR, HOMA-beta-cell and adiponectin concentrations than AGA children. However, in a separate analysis of subjects older than 3 years of age, SGA children showed higher HOMA-IR after adjusting for sex, age and body mass index (BMI) standard deviation score (SDS). Circulating adiponectin was higher in SGA children [adjusted means: 14.5 mg/l (95% CI 12.9-16.1) and 18.7 mg/l (95% CI 17.0-20.3) for AGA and SGA children, respectively; P < 0.0001]. Further analysis revealed that the group of overweight SGA (arbitrarily defined as being in the higher quartile for the BMI SDS distribution in the sample) had decreased serum concentrations of adiponectin, compared to lean SGA children [adjusted means: 12.9 mg/l (95% CI 9.3-16.5) vs. 19.0 (95% CI 16.8-21.3), respectively; P = 0.001]. In a multiple regression model, HOMA-IR and SGA status explained 35% and 15% of adiponectin variance, respectively.
Conclusions:
Prenatal growth restriction is associated with insulin resistance but relatively increased adiponectin concentrations, provided overweight does not ensue. The contributions of circulating adiponectin to the increased risks for developing insulin resistance and type-2 diabetes in formerly SGA subjects merit further studies.
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