Characterization of the insulin-like growth factor axis in term pregnancies complicated by maternal obesity.
OBJECTIVE
Does maternal obesity affect insulin-like growth factor (IGF) axis protein expression patterns in maternal and cord blood?


CONCLUSIONS
Maternal obesity attenuates cord blood expression of IGF-binding protein (IGFBP)-4.


BACKGROUND
The IGF axis plays a critical role in fetal growth and development. Maternal obesity compromises IGF axis protein expression in fetal circulation, which is consistent with the findings of epidemiological studies suggesting that maternal obesity has an independent effect on fetal growth signals during in utero development.


METHODS
This cross-sectional case-control study involved 12 lean [body mass index (BMI) 18.5-24.9 kg/m2] and 12 obese (BMI≥30 kg/m2) women and their neonates at term. At the completion of the study, IGF axis protein expression and hormone concentrations in both maternal and cord blood were examined.


METHODS
We obtained fasting serum samples from cases and controls matched for age, gestation, mode of delivery, parity and glucose tolerance prior to and immediately following elective caesarean section. The corresponding umbilical cord blood was also collected at birth.


RESULTS
Between-group comparisons revealed elevated maternal insulin (P=0.03) and leptin (P<0.01) concentrations in obese gravidas. After adjustment, the maternal homeostasis model of assessment-insulin resistance (HOMA-IR) score was positively correlated with both maternal BMI and leptin levels (P<0.01). Umbilical cord blood levels of IGFBP-3 showed an inverse trend to maternal HOMA-IR (P=0.03) but were directly related to the fetal-placental weight ratio (P<0.01). In cord serum from obese mothers, IGFBP-4 expression was attenuated compared with the controls (P<0.05).


CONCLUSIONS
The limitations of our study include the cross-sectional design and relatively small sample size.


CONCLUSIONS
Our results provide preliminary evidence for the applicability of our findings to other ethnic groups when pregnancy is complicated by obesity.


BACKGROUND
This work was supported by the University of Ottawa, Faculty of Health Sciences/Children's Hospital of Eastern Ontario Research Partnership Grant awarded to K.B.A. and Z.M.F. The authors have no conflicts of interest to declare.
Faculty of Health Sciences, School of Human Kinetics, University of Ottawa, and Healthy Active Living and Obesity Research Group, Children's Hospital of Eastern Ontario Research Institute, Ottawa, Canada.
Z M
ZM
Ferraro
Q
Q
Qiu
A
A
Gruslin
K B
KB
Adamo
D000328:Adult; D015992:Body Mass Index; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D020869:Gene Expression Profiling; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000378:metabolism; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000378:metabolism; D018974:Insulin-Like Growth Factor Binding Protein 4 / Q000378:metabolism*; D020738:Leptin / Q000378:metabolism; D009765:Obesity / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications; D013002:Somatomedins / Q000378:metabolism*
D007328:Insulin; D018970:Insulin-Like Growth Factor Binding Protein 1; D018972:Insulin-Like Growth Factor Binding Protein 3; D018974:Insulin-Like Growth Factor Binding Protein 4; D020738:Leptin; D013002:Somatomedins; D005947:Glucose