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Letters to the Editor |
Department of Gynecology, Obstetrics and, Reproductive Medicine, University of Messina, Messina, Italy
aAddress correspondence to this author at: University of Messina, via setajoli n. 15, 98121 Messina, Italy. Fax 30 90 695201; e-mail rosariodanna{at}tin.it.
To the Editor:
Adiponectin is an adipose tissue–derived protein with important metabolic effects and a strong correlation with insulin sensitivity. In pregnancy there is a progressive increase of insulin resistance, whereas plasma adiponectin concentrations decrease in the 2nd half of gestation (1). In contrast, cord plasma adiponectin concentrations increase throughout gestation (2). Nothing is known about the concentration, origin, or role of amniotic fluid adiponectin, particularly in relation to amniotic insulin. Therefore we evaluated adiponectin and insulin concentrations in the midtrimester amniotic fluid of women with normal pregnancies.
Beginning January 1, 2006, we selected the first 50 pregnant women who underwent a midtrimester amniocentesis for prenatal diagnosis (15–18 weeks gestation) and were found to have a normal pregnancy, defined as an uncomplicated pregnancy with full-term delivery of an infant of adequate size for gestational age. The study was approved by the institutional review board, and all women gave written informed consent.
Amniotic fluid samples were obtained by transabdominal amniocentesis and collected in 15 mL dry tubes. All samples were free of blood contamination, as estimated by microscopic inspection. The samples were immediately centrifuged for 10 min at 3000g and stored at –70 °C. Plasma EDTA samples were centrifuged for 15 min at 1000g within 30 min of collection and stored at –70 °C. Plasma samples required 200-fold dilution before assay. The adiponectin concentration was measured by immunoenzymatic assay (R&D Systems). The intra- and interassay imprecision (CVs) for adiponectin at a concentration of 15.0 µg/L were 3.5% and 5.5%, respectively. The intra- and interassay imprecision values (CVs) for insulin at a concentration of 4.0 mIU/L were 3.3% and 5.6%, respectively.
Amniotic and plasma adiponectin and amniotic insulin concentrations are presented as the median and the 25th–75th percentile range; all other variables are presented as the mean (SD). The Mann–Whitney U-test was used to compare continuous variables between the 2 groups. Univariate correlations between amniotic fluid adiponectin and all the other variables were assessed using the Spearman test. The statistical analysis was performed using SPSS 13.0 (SPSS Inc.). All tests were 2-sided; a P value <0.05 was considered statistically significant.
The clinical characteristics of pregnant women are reported in Table 1
. Median adiponectin amniotic fluid values were 26.8 (13.9–37.3) µg/L, but when we dichotomized for sex, there was a significant difference (P = 0.01) between female 34.8 (18.2–48.7) µg/L and male fetuses 18.2 (13.4–26.8) µg/L. Univariate analysis showed a positive correlation between amniotic adiponectin and insulin (r = 0.47, P = 0.001) and also with gestational age at amniocentesis (r = 0.31, P = 0.03); in contrast amniotic fluid adiponectin did not correlate with plasma adiponectin (r = 0.07, P = 0.6), with maternal age (r = 0.01, P = 0.9), with maternal body mass index (BMI) (r = –0.07, P = 0.5), with gestational age at delivery (r = –0.15, P = 0.1), or with birth weight (r = 0.05, P = 0.7).
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To our knowledge, this is the first study that deals with amniotic fluid concentrations in normal pregnancy at the time of midtrimester amniocentesis. Our results suggest that amniotic adiponectin might be of fetal origin. Maternal origin seems unlikely because there was no correlation between plasma and amniotic adiponectin or between amniotic adiponectin and maternal age or BMI. In addition, Corbetta et al. (3) found no adiponectin in placental tissue. Thus, a fetal origin of amniotic adiponectin appears likely; insulin production by the human fetus from 11 weeks of gestational age has been demonstrated in an experimental study (4), and we have shown a strong correlation between amniotic adiponectin and amniotic insulin. Furthermore, the statistically significant difference between female and male fetuses supports the theory that amniotic adiponectin is of fetal origin. Clinical and experimental studies have demonstrated that the sex dimorphism of adiponectin concentrations might be caused by testosterone-induced inhibition of its secretion from adipocytes (5).
In conclusion, based on our study of 50 normal pregnancies at the time of midtrimester amniocentesis, we suggest that adiponectin found in amniotic fluid is of fetal origin.
Acknowledgments
Grant/funding support: This study has been funded by the University of Messina, Italy.
Financial disclosures: None declared.
References
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