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Markers of Insulin Sensitivity in 12-Year-Old Children Born from Preeclamptic Pregnancies
Satu Seppä1, Raimo Voutilainen2, Sirpa Tenhola1
1Department of Pediatrics, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland; Department of Pediatrics, Kymenlaakso Central Hospital, Kotka, Finland.
Insights
Maternal preeclampsia did not impact offspring insulin sensitivity by age 12. However, the lowest insulin sensitivity group showed higher triglycerides and systolic blood pressure, indicating potential metabolic syndrome clustering.
Area of Science:
- Pediatric Endocrinology
- Metabolic Health
- Pregnancy Complications
Background:
- Maternal preeclampsia is a significant pregnancy complication.
- Its long-term effects on offspring metabolic health, including insulin sensitivity, require further investigation.
Purpose of the Study:
- To investigate the influence of maternal preeclampsia on offspring insulin sensitivity (IS) and related biochemical markers at age 12 years.
Main Methods:
- A case-control study comparing 60 children born to preeclamptic mothers (PRE) with 60 controls (non-PRE).
- Insulin sensitivity was assessed using the Quantitative Insulin Sensitivity Check Index (QUICKI).
- Serum levels of adiponectin, leptin, IGF-1, IGF-2, IGFBP-1, lipids, and blood pressure were measured.
Main Results:
- No significant differences in mean QUICKI or most biochemical markers were observed between PRE and non-PRE groups.
- Within the PRE group, offspring with the lowest IS (lowest QUICKI tertile) exhibited higher serum leptin, triglyceride, IGF-1 levels, and systolic blood pressure.
- Logistic regression confirmed associations between higher leptin, triglyceride, IGF-1, and systolic BP with lower QUICKI in the PRE group.
Conclusions:
- Maternal preeclampsia did not lead to reduced offspring insulin sensitivity by age 12.
- Offspring with the lowest insulin sensitivity showed a clustering of metabolic syndrome components, including elevated triglycerides and systolic blood pressure.
Objective:
To determine whether maternal preeclampsia influences insulin sensitivity (IS) or its biochemical markers in offspring.
Study Design:
Sixty children born from a preeclamptic pregnancy (PRE) and 60 matched control subjects born from a normotensive pregnancy (non-PRE) were studied at age 12 years. IS was estimated using the Quantitative Insulin Sensitivity Check Index (QUICKI), and serum concentrations of adiponectin, leptin, insulin-like growth factor (IGF)-1, IGF-2, IGF-binding protein-1 (IGFBP-1), sex hormone-binding globulin, lipids, and casual blood pressure (BP) were measured.
Results:
The mean values of QUICKI, serum adiponectin, leptin, IGF-1, IGF-2, IGFBP-1, and sex hormone-binding globulin did not differ between the PRE group and non-PRE group (P > .05 for all). The PRE subjects with the lowest IS (the lowest QUICKI tertile; n = 20) had significantly higher mean serum leptin (P = .007), triglyceride (P = .008), and IGF-1 (P = .005) levels and systolic BP (P = .019), and lower serum IGFBP-1 level (P = .007) compared with PRE subjects with higher QUICKI values (n = 40). Similarly, in logistic regression analysis, higher serum leptin (OR, 1.2; P = .009), triglyceride (OR, 1.2; P = .040), and IGF-1 (OR, 1.1; P = .031) levels and systolic BP (OR, 5.8; P = .024) were associated with low QUICKI in the PRE group.
Conclusion:
Maternal preeclampsia did not produce decreased IS in offspring by age of 12 years. However, the offspring with the lowest IS had higher mean serum triglyceride level and systolic BP, suggesting that components of the metabolic syndrome may cluster in this subgroup.
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