期刊
JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION
卷 13, 期 1, 页码 53-57出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jsgi.2005.10.003
关键词
fetal adiposity; cytokines; growth factors; obesity; pregnancy
资金
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R29HD022965, R01HD022965] Funding Source: NIH RePORTER
- NCRR NIH HHS [M0-1-RR-080.] Funding Source: Medline
- NICHD NIH HHS [HD-22965] Funding Source: Medline
- BHP HRSA HHS [P-50-DH11089] Funding Source: Medline
Fetal overgrowth and higher adiposity are hallmarks of pregnancy with maternal obesity and poor glucose tolerance, two conditions associated with decreased maternal insulin sensitivity. In non-pregnant individuals, adipokincs, vasoactive peptides, and components of the immune system crosstalk with metabolic factors to generate signals triggering obesity and impaired insulin action. We have investigated circulating maternal and fetal cytokines and growth-factors as potential biochemical markers of fetal adiposity. Mothers and neonates were classified into three tertiles (T1-T3) using total neonatal fat inass as the outcome with 309 +/- 25g in T1, 478 +/- 40g in T2, and 529 +/- 39g in T3. Umbilical cord endothelin-1 (ET-1), C-peptide, and leptin were higher in T3 and T2 versus T1. Only cord leptin was strongly associated with fetal fat inass (P < . 0 1), whereas neonatal lean body inass was negatively correlated with maternal insulin-like growth factor binding protein-I (IGFBP-I) (r = -0.53, 13 < .04). This study shows an association between in creased fetal adiposity and maternal systemic interleukin-6 (IL-6). No such correlation was found with factors circulating in cord blood, suggesting that the stimuli favoring fetal fat accretion derive from maternal or placental sources rather than from the fetus.
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