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Published on: June 29, 2013
Perinatal changes of plasma resistin concentrations in pregnancies with normal and restricted fetal growth
Despina D Briana1, Maria Boutsikou, Stavroula Baka
1Second Department of Obstetrics and Gynecology, Athens University Medical School, Athens, Greece.
Insights
Resistin levels did not differ between intrauterine growth-restricted (IUGR) and appropriate-for-gestational-age (AGA) neonates. This suggests resistin may not directly regulate insulin sensitivity or adipogenesis during the perinatal period.
Area of Science:
- Endocrinology
- Metabolic Syndrome
- Perinatal Medicine
Background:
- Resistin, an adipocytokine, inhibits adipogenesis and promotes insulin resistance.
- Intrauterine growth restriction (IUGR) is linked to reduced fat mass and metabolic changes, increasing adult insulin resistance risk.
- Investigating resistin in IUGR is crucial for understanding long-term metabolic health.
Purpose of the Study:
- To determine plasma resistin concentrations in maternal, fetal, and neonatal samples from IUGR and appropriate-for-gestational-age (AGA) pregnancies.
- To correlate resistin levels with insulin concentrations in these groups.
- To explore the influence of IUGR on resistin and insulin dynamics.
Main Methods:
- Plasma resistin and insulin levels were measured in 40 mothers and their 20 IUGR and 20 AGA singleton neonates.
- Samples were collected on postnatal days 1 (N1) and 4 (N4).
- Statistical analyses were performed to compare groups and assess correlations.
Main Results:
- No significant differences in resistin concentrations were found between AGA and IUGR groups.
- Maternal resistin levels were lower than fetal/neonatal levels in AGA, and lower than N1 levels in IUGR.
- No correlation was observed between resistin and insulin concentrations in either group.
Conclusions:
- Resistin concentrations do not differ between IUGR and AGA neonates, suggesting it may not directly regulate perinatal insulin sensitivity or adipogenesis.
- The lack of correlation between resistin and insulin implies distinct regulatory pathways.
- Mode of delivery and parity do not impact circulating resistin levels.
Background:
The adipocytokine resistin inhibits adipogenesis and induces insulin resistance. Intrauterine growth-restricted (IUGR) neonates have reduced fat mass and changes of endocrine/metabolic mechanisms, predisposing to insulin resistance and metabolic syndrome in adult life.
Objectives:
To investigate plasma resistin concentrations in maternal, fetal and neonatal samples from IUGR and appropriate-for-gestational-age (AGA) pregnancies and correlate them with respective insulin concentrations.
Methods:
Plasma resistin and insulin concentrations were determined in 40 mothers and their 20 IUGR and 20 AGA singleton full-term fetuses and neonates on postnatal day 1 (N1) and day 4 (N4).
Results:
No significant differences in resistin concentrations were observed between AGA and IUGR groups. In the AGA group, maternal resistin concentrations were significantly lower compared to fetal, N1 and N4 ones (p = 0.003, p = 0.017 and p = 0.039, respectively). Maternal resistin concentrations positively correlated with fetal ones (r = 0.527, p = 0.02). In the IUGR group, maternal resistin concentrations were significantly lower compared to N1 (p < 0.001) and positively correlated with N4 concentrations (r = 0.626, p = 0.007). In both groups, the effect of gender, mode of delivery, parity and adjusted birth weight (customized centiles) on resistin concentrations was not significant. No correlation between resistin and insulin concentrations was documented.
Conclusions:
Lack of difference in resistin concentrations between IUGR and AGA groups, and lack of correlation between resistin and insulin concentrations as well as customized centiles, possibly suggests that resistin may not be directly involved in the regulation of insulin sensitivity and adipogenesis in the perinatal period. Mode of delivery and parity are not associated with circulating resistin concentrations.
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