Both intrauterine growth restriction and postnatal growth influence childhood serum concentrations of adiponectin.
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).


METHODS
Cross-sectional, hospital-based study dealing with insulin sensitivity in SGA children.


METHODS
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).


METHODS
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.
López-Bermejo
Abel
A
Diabetes, Endocrinology and Nutrition Unit, Dr Josep Trueta Hospital of Girona, Girona, Spain. uden.alopez@htrueta.scs.es
Casano-Sancho
Paula
P
Fernández-Real
José Manuel
JM
Kihara
Shinji
S
Funahashi
Tohru
T
Rodríguez-Hierro
Francisco
F
Ricart
Wifredo
W
Ibañez
Lourdes
L
D052242:Adiponectin; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003430:Cross-Sectional Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000097:blood*; D006128:Growth; D006706:Homeostasis; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008055:Lipids / Q000097:blood; D016015:Logistic Models; D008297:Male
D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D008055:Lipids