Maternal serum adiponectin multimers in patients with a small-for-gestational-age newborn
Objective: Several mechanisms of disease have been implicated in the pathophysiology of small-for-gestational-age (SGA) including an anti-angiogenic state, and an exaggerated intravascular pro-inflammatory response. Adiponectin plays a role in a wide range of biological activities including those that have been implicated in the pathophysiology SGA. Thus, the aim of this study was to determine if third trimester adiponectin concentrations differed between women with normal weight infants and those with an SGA neonate. Study design: This cross-sectional study included women with: 1) a normal pregnancy (n=234); and 2) an SGA neonate (n=78). SGA was defined as a birth weight below the 10th percentile for gestational age at birth. The study population was further stratified by first trimester body mass index (BMI) (normal weight <25 kg/m2 vs. overweight/obese ≥25 kg/m2). Maternal serum adiponectin multimers [total, high-molecular-weight (HMW), medium-molecular-weight (MMW) and low-molecular-weight (LMW)] concentrations were determined by ELISA. Non-parametric statistics were used for analyses. Results: 1) The median maternal serum concentrations of total, HMW and MMW adiponectin were significantly lower in patients with an SGA neonate than in those with normal pregnancies; 2) patients with an SGA neonate had a significantly lower median HMW/total adiponectin ratio and higher median MMW/total adiponectin and LMW/total adiponectin ratios than those with a normal pregnancy; 3) among patients with an SGA neonate, neither maternal serum concentrations of adiponectin multimers, nor their relative distribution differ between normal weight and overweight/obese patients. Conclusion: 1) Pregnancies complicated by an SGA neonate are characterized by a alterations in the maternal serum adiponectin multimers concentrations and their relative abundance; 2) the findings reported herein suggest that maternal adipose tissue may play a role, in the pathogenesis of SGA.
