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The 4-vessel Sampling Approach to Integrative Studies of Human Placental Physiology In Vivo
Published on: August 2, 2017
Cord blood ASP is predicted by maternal lipids and correlates with fetal birth weight
Jumana Saleh1, Hamed D S Al-Riyami, Taqdees A Chaudhary
1Department of Biochemistry, Sultan Qaboos University, Muscat, Oman. jumana@squ.edu.om
Background:
The acylation stimulating protein (ASP) is a potent lipogenic adipokine that correlates with postprandial triglyceride (TG) clearance and is linked to the pathophysiology of obesity and related disorders.
Objective:
To investigate ASP levels in cord blood and its relation to maternal and cord blood lipid parameters and fetal birth weight.
Methods And Procedures:
Thirty nondiabetic pregnant women, their newborns, and thirty-three nonpregnant controls were included in this study. Fasting maternal and cord blood ASP, TGs, nonesterified fatty acids (NEFAs), cholesterol, glucose levels, in addition to maternal BMI and fetal birth weight were measured.
Results:
No significant difference was found between cord blood ASP (16.3 +/- 0.96 nmol/l) and ASP levels in the adult controls (15.7 +/- 1.0 nmol/l). Cord blood ASP, however, was lower than maternal plasma ASP levels (25.4 +/- 1.6 nmol/l, P < 0.001). Yet, lipid levels in cord blood, particularly TGs were markedly decreased compared to control and maternal TG levels (threefold and 7.4-fold, P < 0.001 respectively). Maternal TGs significantly correlated with fetal birth weight (r = 0.54, P = 0.002). Multiple regression analysis showed that maternal TGs (beta = 0.57, P = 0.01) and NEFAs (beta = 0.43, P = 0.024) predicted 45% variation in cord blood ASP levels, independent of all measured maternal and cord blood parameters. Cord blood ASP showed a positive correlation with fetal birth weight (r = 0.524, P = 0.037) in neonates above average fetal birth weight of the studied population.
Discussion:
This is the first study investigating ASP in cord blood. We suggest that maternal hypertriglyceridemia is associated with increased fetal ASP production, thus enhancing fetal fat storage independent of maternal glucose variations in nondiabetic women.
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