Maternal and foetal resistin and adiponectin concentrations in normal and complicated pregnancies

University of Milan, Milano, Lombardy, Italy
Clinical Endocrinology (Impact Factor: 3.35). 04/2007; 66(3):447-53. DOI: 10.1111/j.1365-2265.2007.02761.x
Source: PubMed

ABSTRACT The aim of this study was to evaluate how resistin and adiponectin (ApN) are involved in maternal energy metabolism and foetal growth.
A cross-sectional study.
Resistin and ApN were measured in 30 healthy nonpregnant women, 73 pregnant women [10-41 weeks of gestation; 18 with gestational diabetes mellitus (GDM), five with pregnancy-induce hypertension (PIH), nine with pre-eclampsia (PE), eight with chronic hypertension (CH) and 33 normal] and 40 foetal samples (20-41 weeks of gestation; 18 from GDM mothers and 22 from normal mothers).
Resistin levels were significantly higher in normal pregnant women than in nonpregnant controls (13.7 +/- 2.1 vs. 6.3 +/- 1.6 ng/ml; P < 0.005) and showed a negative correlation with gestational age (P < 0.0001, r = -0.7). Only women with PE presented resistin levels significantly lower than normotensive women of the same gestational age (8.2 +/- 1.2 vs. 17.9 +/- 4.3 ng/ml; P < 0.005). ApN levels, although similar in normal pregnant women to those in nonpregnant controls, were significantly lower in women with GDM (37-41 weeks; 5.2 +/- 0.5 vs. 8.2 +/- 0.8 mg/l; P < 0.0001) and PE (20-37 weeks; 5.0 +/- 0.7 vs. 9.5 +/- 0.7 mg/l; P = 0.008) than those found in normal women matched for gestational age. Resistin was detected in the umbilical venous blood in foetuses from 20 to 41 weeks of gestation. In all newborns, both resistin and ApN levels were significantly higher than those recorded in adult life and did not correlate with maternal levels (P = ns, r = 0.03 for resistin and P = ns, r = -0.3 for ApN). Foetuses from diabetic mothers had ApN significantly lower than normal foetuses (26.8 +/- 2.6 vs. 37.5 +/- 3.5 mg/l; P = 0.02), while resistin levels were similar (17.3 +/- 3.7 vs. 18.2 +/- 1.5 ng/ml; P = ns).
The secretion pattern of ApN in normal and complicated pregnancies strongly suggests an involvement of ApN in insulin resistance during gestation, while resistin seems to have a minor role. Moreover, the detection of high levels of resistin and ApN in cord blood during gestation is consistent with a regulatory action of these adipokines on tissue differentiation and foetal growth.

Download full-text


Available from: Anna Maria Marconi, Sep 02, 2014
  • Source
    • "Resistin levels increase along gestation [15] and its concentration is higher in pregnant women than in non-pregnant subjects [16]. However, the role of resistin in GDM remains controversial and the results from different studies are inconclusive [8] [17] [18]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective Adipokines play an important role in the pathogenesis of insulin resistance during pregnancy. We studied the association of genetic variants linked with type 2 diabetes in gestational diabetes mellitus (GDM) subjects and its influence on maternal adipokines. Study Design We recruited 25 healthy pregnant women (Controls) and 45 women with GDM at 24-28 weeks of gestation. Maternal blood samples were collected at recruitment and delivery. Adipokines were determined at both sampling times. Genomic DNA was extracted from recruitment samples and FTO rs9939609, TCF7L2 rs4506565, rs7901695, rs12243326, rs12255372 and rs7903146, INSIG2 rs7566605, SREBF1 rs114001633, rs45535737 and rs12941356 and FATP4 rs2003560 genotyped. Results Serum adiponectin was significantly lower in GDM than Controls at recruitment and showed a similar trend at delivery (p = 0.060). In contrast, resistin tended to higher levels in GDM only at recruitment. TCF7L2 rs4506565 (OR = 2.31, 95% CI:1.97-5.01; p = 0.031) and FTO rs9939609 (OR = 2.17, 95% CI: 1.07-4.41; P = 0.039) were associated with GDM risk. Women carrying the T allele of TCF7L2 rs4506565 had increases in plasma resistin of 9.38 μg/L (95% CI 1.39-17.37; p = 0.022) per allele; this association remained significant after adjusting for pre-gestational body weight. Conclusion TCF7L2 rs4506565 variant (T/T) is associated with increased risk of GDM and plasma resistin concentrations in women with GDM.
    European Journal of Obstetrics & Gynecology and Reproductive Biology 09/2014; 180. DOI:10.1016/j.ejogrb.2014.06.024 · 1.63 Impact Factor
  • Source
    • "In the present study, adiponectin was signifi cantly reduced in patients with adverse pregnancy outcomes in the whole cohort. Although there are confl icting results, lower levels of adiponectin have been reported in pre-eclampsia and IUGR, as well as in GDM (Cortelazzi et al. 2007; Ouyang et al. 2007; Kyriakakou et al. 2008). It was demonstrated that in patients with reduced adiponectin levels, there is also an increased risk of fetal overgrowth (Tsai et al. 2005; Nanda et al. 2011). "
    [Show abstract] [Hide abstract]
    ABSTRACT: We investigated adiponectin levels in women with gestational diabetes mellitus (GDM) and normal glucose tolerance (NGT) at 24-28 gestational weeks. Fasting serum adiponectin, glucose and glycated haemoglobin (HbA1c) were determined in 88 pregnant women, 44 with GDM and 44 with NGT. Pre-pregnancy and current body mass indices (BMI), weight gain and pregnancy outcomes were investigated. Serum adiponectin was significantly reduced in GDM compared with the NGT group (p = 0.000). Adiponectin was negatively correlated with age (r = -0.419, p = 0.000); glucose (r = -0.263, p = 0.013); HbA1c (r = -0.274, p = 0.01); BMI (pre-pregnancy and current) (r = -0.317, p = 0.003 and r = -0.303, p = 0.004) and positively correlated with gestational age at delivery (r = 0.278, p = 0.009). The GDM group delivered significantly earlier than the NGT group (p = 0.001). Adverse pregnancy outcomes and abdominal delivery were higher in the GDM group (p = 0.000, p = 0.033, respectively), and adiponectin was significantly reduced in patients with adverse outcomes (p = 0.003) and abdominal delivery (p = 0.032). Adiponectin is reduced in patients with GDM. Association of adiponectin with adverse pregnancy outcomes remains to be elucidated.
    Journal of Obstetrics and Gynaecology 04/2014; 34(6). DOI:10.3109/01443615.2014.902430 · 0.60 Impact Factor
  • Source
    • "During the course of pregnancy, maternal adiponectin secretion gradually declines [12]. In PE, a paradoxical and significant increase of circulating adiponectin of 30% to 87% has been described in most [6, 13– 15] but not all studies [16] [17]. PE could be characterized into 2 different disease entities: early-onset PE (EOPE) and late-onset PE (LOPE) which is associated with different fetal and maternal effects, heritability , biochemical markers, and clinical symptoms [18]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Aim. This study was designed to clarify the role of leptin and adiponectin in preeclampsia (PE) pathogenesis and different subtypes of preeclampsia. Method. This case control study was performed in 45 PE patients and 45 healthy controls matched for age, BMI, and ethnicity. Serum leptin and adiponectin levels were determined by enzyme linked immunosorbent assay (ELISA). Results. Maternal serum leptin and adiponectin were significantly higher in PE women than controls. Serum leptin was elevated in early onset preeclampsia (EOPE) and late onset preeclampsia (LOPE) compared to controls. Among PE patients, serum leptin was higher in EOPE than LOPE women. However, serum adiponectin was not different between EOPE and LOPE women. The serum leptin was significantly higher in severe PE than mild PE. The serum adiponectin was significantly elevated in severe PE compared to controls. Significant positive correlation was observed between leptin and adiponectin and also between leptin and BMI in controls. Moreover significant positive correlation was observed between adiponectin and BMI in PE patients and controls. Conclusion. The present study showed that serum leptin level may play a significant role as a biomarker to differentiate early and late onset PE and also its relation to BMI and severity of disease.
    Disease markers 01/2014; 2014:628476. DOI:10.1155/2014/628476 · 2.17 Impact Factor
Show more