A Review of Maternal and Fetal Growth Factors in Diabetic Pregnancy

Higgins, Mary; Auliffe, Fionnuala Mc

doi:10.2174/157339910790909431

Cited by 71 publications

(51 citation statements)

References 108 publications

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“…It has been demonstrated that cord blood concentrations of leptin and adiponectin are associated to subsequent BMI and central adiposity in children (21). Therefore, whereas the clinical applications of this data remain speculative, it may be possible that neonatal levels of adipokines and particularly their mutual relationship could be used to identify neonates with increased risk of developing childhood obesity and/or its related complications.…”

Section: Discussionmentioning

confidence: 99%

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Adipokines in umbilical cord blood from children born large for gestational age

Lausten-Thomsen¹,

Christiansen

Hedley

et al. 2016

Journal of Pediatric Endocrinology and Metabolism

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Background: The etiology of childhood obesity and the associated morbidity is multifactorial. Recently, data suggesting a prenatal programming towards later childhood obesity and metabolic deregulation through the intrauterine environment has emerged. This study explored the concentrations of adipokines and their mutual relationship at birth in children born to non-diabetic mothers. Methods: Adiponectin, leptin and sOB-R were measured using ELISA-based commercial kits in umbilical cord blood from 60 neonates (30 born large for gestational age [LGA] and 30 born appropriate for gestational age [AGA]). Children exposed to maternal diabetes, chronic disease and preeclampsia were excluded. Results: The LGA group exhibited significantly elevated concentrations of leptin (p < 0.001) and of free leptin index (p < 0.001) and decreased sOB-R concentrations (p = 0.005) when compared to the AGA group, which persisted in multiple regression analysis after taking the gestational age into account (p = 0.048, p < 0.001 and p < 0.001, respectively). Only a trend towards a difference in adiponectin was demonstrated (p = 0.057) regardless of adjustment (p = 0.150). However, the leptin/adiponectin ratio was

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Section: Discussionmentioning

confidence: 99%

“…Leptin appears to play a role in a number of processes associated with pathological fetal growth, most notably maternal diabetes (21,22). Leptin in umbilical cord blood has been demonstrated to be of fetal origin as it is independent of maternal levels of leptin (23).…”

Section: Introductionmentioning

confidence: 99%

Adipokines in umbilical cord blood from children born large for gestational age

Lausten-Thomsen¹,

Christiansen

Hedley

et al. 2016

Journal of Pediatric Endocrinology and Metabolism

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“…Increased fetal weight in the infants of diabetic mothers was previously considered to be the result of maternal hyperglycemia. However, the control of fetal growth in pregnancies with or without underlying diabetes is significantly more complicated (8).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of oral glucose tolerance test, β-cell function and adverse obstetric outcomes

et al. 2013

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Abstract. This study was conducted in order to investigate the prevalence of impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM), their effect on pregnancy and their association with adverse obstetric outcomes. A cross-sectional study was performed on 345 pregnant women, who were screened between the 24th and 28th gestational week with a 75-g oral glucose tolerance test following abnormal results at 1 h after a 50-g oral glucose challenge test. The obstetric outcomes were recorded along with plasma glucose and insulin levels, homeostasis model assessment of insulin resistance (HOMA-IR) and homeostasis model assessment of β-cell function index (HOMA-βCFI) and 50 subjects were excluded due to incomplete data recovery. Of the 295 pregnant women, 18.6% (55/295) were diagnosed with GDM and 32% (95/295) with IGT. The GDM group exhibited significantly higher fasting and 1-h blood glucose concentrations compared to the normal glucose tolerance (NGT) and IGT groups (P<0.01). The 2-and 3-h insulin values of the NGT group were significantly lower compared to those of the GDM group (P<0.05, P<0.01). In the IGT group, the 2-h insulin values were higher compared to the NGT group and the 3-h values were significantly higher (P<0.01), similar to the GDM group. There was a tendency for progressively decreased β-cell function and increased HOMA-IR from the NGT to the IGT to the GDM group. The adverse outcomes of pregnancy-induced hypertension, fetal distress, neonatal hyperbilirubinemia, preterm delivery, macrosomia and cesarean delivery indicated an association with HOMA-βCFI and HOMA-IR. In conclusion, these findings suggest a clinical significance of β-cell dysfunction in women with gestational IGT.

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“…When we perform prospective sampling at defined time intervals we have data that show good correlation with IGF-1/2 levels and birth weight but not with IGFBP-1 and -3 [23,24,37]. Later studies conclude that IGF-1/2 cannot solely explain the complex process of fetal growth, as it is influenced by maternal glycemia as well as genetics, diabetic factors, maternal and fetal hormones [38].…”

Section: Temporal Review Of Studies On Fetal Growth and The Igf Systemmentioning

confidence: 95%

Macrosomia and the IGF System: A Short Review

Al-Far¹,

Tjessem²,

Lauszus³

2017

Foc Sci

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Introduction: Macrosomia in diabetic pregnancy is an ubiquitous finding and implies both maternal and fetal issues. Its incidence surpasses other critical obstetrical morbidity in diabetic pregnancy with increased placental size and polyhydramnios as comorbidity. The studies on the underlying factors contributing to macrosomia have focused on growth stimuli like IGF, glycemia, and insulin and their effects on regional organ function. IGF-I and -II in maternal serum are associated with birth weight and the bioavailabiliy is modulated by IGF-binding-proteins (IGFBP) and phosporylated isoforms of IGFBP and the presence of proteases and IGF split products. Human placental growth hormone regulates the effect of IGF-I in pregnancy. Methods: The literature on the IGF system′s possible effect on fetal growth in diabetic pregnancy is reviewed before our current studies and updated with respect to later findings. Regulation on bioavailability by proteolysis and phosporylation is described. The review discusses briefly the studies on pregnant women with type 1 diabetes with respect to vasculopathy. Results: The data show good correlation of IGF-1/2 levels with birth weight. No such correlation with IGFBP-1 and -3 is found. Fetal growth deviation in diabetic pregnancy is not uniform. In first trimester, growth delay is documented in fetal growth curves compared to non-diabetic controls. Accordingly, a shift in IGF-IGFBP regulation in second trimester is found with less proteolysis of IGFBPs and relative increase in total binding capacity. In third trimester, free IGF further increases as IGFBP binding decreases by proteolysis and modulation. The first trimester values may be used as predictor of fetal weight at term. Diabetic women show a two-to threefold increase in the in vitro IGFBP-3 proteolytic activity during pregnancy as compared to post-partum values. Conclusions: Prominent proteolysis of binding proteins and the modulation by insulin account for the mechanism leading to macrosomia. The two factors combined guarantee the stimulation by more bioavailable IGF and the glycemic levels reveal whether insulin dose are optimal. Structural factors of diabetes i.e. microangiopathy further modulate the sum of effects on fetal growth. In contrast to macrosomia, fetal growth restriction is associated with prominent maternal vascular endothelial complications, such as overt nephropathy, proliferative retinopathy, preeclampsia, and hypertension. In parallel to the growth inhibition, stimulatory effects are exerted by the GH axis including the placental growth hormones and occur probably as compensatory mechanism, similar to the increased IGFBP-3 proteolysis in late pregnancy found in growth retardation. This influence may in part explain the disproportionate growth in different tissue components occurring in the various stages of diabetic pregnancy.

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A Review of Maternal and Fetal Growth Factors in Diabetic Pregnancy

Cited by 71 publications

References 108 publications

Adipokines in umbilical cord blood from children born large for gestational age

Adipokines in umbilical cord blood from children born large for gestational age

Evaluation of oral glucose tolerance test, β-cell function and adverse obstetric outcomes

Macrosomia and the IGF System: A Short Review

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