TY  - JOUR
A1  - Li, Jian
A1  - Wang, Zi-Neng
A1  - Schlemm, Ludwig
A1  - Pfab, Thiemo
A1  - Xiao, Xiao-Min
A1  - Chen, You-Peng
A1  - Hocher, Berthold
T1  - Low birth weight and elevated head-to-abdominal circumference ratio are associated with elevated fetal glycated serum protein concentrations
JF  - Journal of hypertension
N2  - Objective To analyze the association between low birth weight, head-to-abdominal circumference ratio, and insulin resistance in early life.
 Method and results Glycated serum proteins (GSPs) were quantified at delivery in 612 Chinese mother/child pairs serving as a surrogate of maternal and fetal glycemia. Differential ultrasound examination of the fetal's body (head circumference, biparietal diameter, pectoral diameter, abdominal circumference, and femur length) was done in average 1 week prior to delivery. Multivariable regression analysis considering gestational age at delivery, the child's sex, maternal BMI, maternal age at delivery, maternal body weight, and pregnancyinduced hypertension revealed that fetal GSP was inversely associated with birth weight (R(2) = 0.416; P < 0.001). Fetal GSP was furthermore positively associated with the head-to-abdominal circumference ratio, whereas the maternal GSP was negatively correlated with the offspring's head-to-abdominal circumference ratio (R(2) = 0.285; P = 0.010 and R(2) = 0.261; P = 0.020, respectively). The increased head-to-abdominal circumference ratio in newborns with higher fetal GSP is mainly due to a reduced abdominal circumference rather than reduced growth of the brain.
 Conclusion The disproportional intrauterine growth is in line with the concept of so-called brain sparing, a mechanism maintaining the intrauterine growth of the brain at the expense of trunk growth. Our data suggest that the low birth weight phenotype, linked to cardiovascular diseases like hypertension in later life, might be a phenotype of disproportional intrauterine growth retardation and early life insulin resistance.
KW  - disproportional intrauterine growth retardation
KW  - insulin resistance
KW  - low birth weight
KW  - ultrasound
Y1  - 2011
U6  - https://doi.org/10.1097/HJH.0b013e328349a2e6
SN  - 0263-6352
VL  - 29
IS  - 9
SP  - 1712
EP  - 1718
PB  - Lippincott Williams & Wilkins
CY  - Philadelphia
ER  - 
TY  - JOUR
A1  - Hocher, Berthold
A1  - Heimerl, Dirk
A1  - Slowinski, Torsten
A1  - Godes, Michael
A1  - Halle, Horst
A1  - Priem, Friedrich
A1  - Pfab, Thiemo
T1  - Birthweight and Fetal Glycosylated Hemoglobin at Birth in Newborns Carrying the GLUT1 XbaI Gene Polymorphism
JF  - Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion
N2  - Background: Low birthweight is an independent risk factor of glucose intolerance and type 2 diabetes in later life. Genetically determined insulin resistance and subsequently impaired glucose uptake might explain both reduced fetal growth and elevated blood glucose. The glucose transporter 1 (GLUT!) plays an important role for fetal glucose uptake as well as for maternal-fetal glucose transfer, and it has been associated with insulin resistance in adults. The present study hypothesized that the common fetal GLUT1 XbaI polymorphism might reduce fetal insulin sensitivity and/or glucose supply in utero, thus affecting fetal blood glucose and fetal growth.
 Methods: A genetic association study was conducted at the obstetrics department of the Charite University Hospital, Berlin, Germany. 119.1 white women were included after delivery, and all newborns were genotyped for the GLUT1 XbaI polymorphism. Total glycosylated hemoglobin was quantified, serving as a surrogate of glycemia during the last weeks of pregnancy.
 Results: The analysis of this large population showed no significant differences in fetal glycosylated hemoglobin or birthweight for the different fetal GLUT1 XbaI genotypes. Only newborns carrying the mutated allele show the previously published inverse association between birthweight and glycosylated hemoglobin.
 Conclusions: The results suggest that there is no prenatal effect of the fetal GLUT1 XbaI polymorphism on fetal insulin sensitivity, intrauterine fetal glucose supply or fetal growth. However, the polymorphism seems to modulate the inverse interaction between birthweight and fetal glycemia.
KW  - GLUT1 XbaI gene polymorphism
KW  - birthweight
KW  - total glycosylated hemoglobin
KW  - insulin resistance
KW  - fetal programming
Y1  - 2011
SN  - 1433-6510
VL  - 57
IS  - 9-10
SP  - 651
EP  - 657
PB  - Clin Lab Publ., Verl. Klinisches Labor
CY  - Heidelberg
ER  -