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First-Trimester Maternal Serum Adiponectin/Leptin Ratio in Pre-Eclampsia and Fetal Growth
Victoria E de Knegt1,2, Paula L Hedley1,3, Anna K Eltvedt1
1Department for Congenital Disorders, Statens Serum Institut, 2300 Copenhagen, Denmark.
Insights
The first-trimester adiponectin/leptin ratio is reduced in pre-eclampsia (PE) pregnancies, indicating impaired insulin sensitivity. This ratio is a better predictor of PE than individual adiponectin or leptin levels.
Area of Science:
- Reproductive endocrinology
- Maternal-fetal medicine
- Metabolic health
Background:
- The serum adiponectin/leptin ratio (A/L ratio) serves as a marker for insulin sensitivity.
- Pre-eclampsia (PE) is linked to maternal metabolic syndrome and potential fetal growth restriction.
- Early pregnancy metabolic markers may predict PE development.
Purpose of the Study:
- To investigate the association between the first-trimester A/L ratio and the development of pre-eclampsia (PE).
- To assess the relationship between the first-trimester A/L ratio and birth weight in pregnancies that develop PE.
- To evaluate the predictive value of the A/L ratio for PE and its clinical severity.
Main Methods:
- Quantification of adiponectin and leptin in first-trimester serum samples from women in the Copenhagen First-Trimester Screening Study.
- Analysis of samples from 126 women who developed PE and 297 controls.
- Multiple logistic regression and correlation analyses to assess associations with PE, birth weight, and clinical severity, adjusting for maternal BMI.
Main Results:
- The A/L ratio was significantly lower in PE pregnancies compared to controls (median 0.17 vs. 0.32, p < 0.001).
- A reduced A/L ratio was negatively associated with PE, independent of maternal BMI (OR = 0.315).
- The A/L ratio demonstrated a higher predictive value for PE (AUC = 0.737) than adiponectin or leptin alone, but was not clinically relevant as a single marker.
- PE was associated with lower relative birth weight, and leptin, not the A/L ratio, was significantly associated with birth weight in PE pregnancies after BMI correction.
Conclusions:
- An impaired first-trimester A/L ratio is characteristic of pre-eclampsia, reflecting underlying metabolic changes.
- Aberrant fetal growth in PE appears to be mediated by leptin-associated pathways rather than insulin sensitivity.
- The A/L ratio may serve as an early indicator of PE risk, but further validation is needed for clinical application.
Abstract:
The serum adiponectin/leptin ratio (A/L ratio) is a surrogate marker of insulin sensitivity. Pre-eclampsia (PE) is associated with maternal metabolic syndrome and occasionally impaired fetal growth. We assessed whether the A/L ratio in first-trimester maternal serum was associated with PE and/or birth weight. Adiponectin and leptin were quantitated in first-trimester blood samples (gestational week 10+3−13+6) from 126 women who later developed PE with proteinuria (98 mild PE; 21 severe PE; 7 HELLP syndrome), and 297 controls, recruited from the Copenhagen First-Trimester Screening Study. The A/L ratio was reduced in PE pregnancies, median 0.17 (IQR: 0.12−0.27) compared with controls, median 0.32 (IQR: 0.19−0.62) (p < 0.001). A multiple logistic regression showed that PE was negatively associated with log A/L ratio independent of maternal BMI (odds ratio = 0.315, 95% CI = 0.191 to 0.519). Adiponectin (AUC = 0.632) and PAPP-A (AUC = 0.605) were negatively associated with PE, and leptin (AUC = 0.712) was positively associated with PE. However, the A/L ratio was a better predictor of PE (AUC = 0.737), albeit not clinically relevant as a single marker. No significant association was found between A/L ratio and clinical severity of pre-eclampsia or preterm birth. PE was associated with a significantly lower relative birth weight (p < 0.001). A significant negative correlation was found between relative birth weight and A/L ratio in controls (β = −0.165, p < 0.05) but not in PE pregnancies), independent of maternal BMI. After correction for maternal BMI, leptin was significantly associated with relative birth weight (β = 2.98, p < 0.05), while adiponectin was not significantly associated. Our findings suggest that an impairment of the A/L ratio (as seen in metabolic syndrome) in the first trimester is characteristic of PE, while aberrant fetal growth in PE is not dependent on insulin sensitivity, but rather on leptin-associated pathways.
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