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

University of Milan, Milano, Lombardy, Italy
Clinical Endocrinology (Impact Factor: 3.46). 04/2007; 66(3):447-53. DOI: 10.1111/j.1365-2265.2007.02761.x
Source: PubMed


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.

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Available from: Anna Maria Marconi, Sep 02, 2014
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    • "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]. "
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    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(1). DOI:10.1016/j.ejogrb.2014.06.024 · 1.70 Impact Factor
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    • "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). "
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    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 · 0.55 Impact Factor
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    • "Oocyte Embryo Pregnancy Leptin " in obesity interferes with follicular and oocyte development [68]; counteracts high glucose effect [70]; " in PCOS, BMI-correlated [71] Embryo implantation and embryomaternal cross-talk [72]; # in human implantation failure [73]; " in LGA and # in SGA infants [74] " during normal pregnancy, # around parturition [75]; "" in obese pregnancy [76], delivery disorders [65]; " in GDM, PE [77], # or $ in GDM [78] Adiponectin Positively correlates with the number of oocytes retrieved in ART [79]; # in PCOS [80] BMI-correlated [71] Preimplantation embryo development [81]; promotes trophoblast invasion [82]; placental nutrient transport [83]; inversely correlates with birth weight [84] # during pregnancy in association to the normal pregnancyrelated insulin-sensitivity [85]; # in GDM [86] and PE [88] Resistin Negatively correlates with ovarian response in ART [89]; $ between obese and non-obese PCOS [90] " as pregnancy progresses [57]; "" [91], # or $ in GDM [78] Visfatin In FF correlates with the number of oocytes retrieved in ART [92]; in plasma positively correlate with BMI and PCOS [93]; coadminis- tration with gonadotropins increases fertility [94] " during pregnancy [95]; # [96] and " [97] in GDM; " in PE [98] Omentin # in obesity [99]; expressed in ovary [100]; # in overweight PCOS [101] Detectable in human fetus; no correlation between serum concentration and birth weight [102]; # maternal obesity, negatively correlates with fetal birth weight [103] # in placenta, plasma e adipose tissue of obese women [103] Vaspin " in obesity and PCOS [104]; $ between obese and non-obese women [105] Detectable in human fetus; no correlation between serum concentration and birth weight [102] $ in GDM, PE and normal pregnancy [106] Chemerin Cord blood levels positively correlates with birth weight [107] " during pregnancy, # to the end [108]; $ in GDM [109]; " in PE [110] TNF-a Impaired levels in FF correlate with oocytes quality [111] and reduced fertilization rate [112] in ART; " levels in PCOS obesity-correlated [114] " during pregnancy [116]; "" in obese pregnancy [117]; " in PE [118] IL-6 " endometriosis-associated, reduces fertilizing oocyte capacity [119]; " in PCOS obesity-correlated [71]; increases oocyte competence in vitro fertilization [120] " during pregnancy [116]; "" in obese pregnancy [117]; " in PE [118] IL-18 " during pregnancy [123]; "" in PE [67] TABLE 1 Santangelo et al. vaspin, and omentin, are also produced by the human reproductive system and contribute to modulate every phases of the reproductive process [4] [5] [49] [56] [57] [66] [67] (Table 1). "
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    ABSTRACT: Obesity is a global and dramatic public health problem; maternal obesity represents one of the main risk factors of infertility and pregnancy complications as it is associated with adverse maternal and offspring outcomes. In the last few years, adipose tissue dysfunction associated with altered adipocytokine secretion has been suggested to play a critical role in all the phases of reproductive process. Obesity is a nutrition-related disorder. In this regard, dietary intervention strategies, such as high intake of fruit and vegetables, have shown significant effects in both preserving health and counteracting obesity-associated diseases. Evidence has been provided that polyphenols, important constituents of plant-derived food, can influence developmental program of oocyte and embryo, as well as pregnancy progression by modulating several cellular pathways. This review will examine the controversial results so far obtained on adipocytokine involvement in fertility impairment and pregnancy complications. Furthermore, the different effects exerted by polyphenols on oocyte, embryo, and pregnancy development will be also taken in account. © 2013 BioFactors, 2013.
    BioFactors 02/2014; 40(1). DOI:10.1002/biof.1126 · 4.59 Impact Factor
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