Maternal Serum and Umbilical Cord Blood Leptin Concentrations With Fetal Growth Restriction

Pighetti, M; Tommaselli, Giovanni A.; D’Elia, A; Carlo, Costantino Di; Mariano, Angela; Carlo, Angela Di; Nappi, Carmine

doi:10.1097/00006250-200309000-00020

Cited by 20 publications

(24 citation statements)

References 21 publications

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“…1). These findings support the report from Pighetti et al that normotensive women with SGA neonates have higher plasma leptin levels than those with AGA neonates [26]. Moreover, in the present study, we clearly demonstrated negative correlation between maternal plasma leptin levels and ∆SD of body weight of neonates in all studied population as well as in non-preeclamptic subjects (Fig.…”

Section: Discussionsupporting

confidence: 93%

The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

et al. 2007

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Abstract. Leptin is a satiety hormone secreted from the adipose tissue and human placenta. We previously demonstrated that severe preeclampsia up-regulated leptin mRNA expression in the placenta and elevated maternal plasma leptin concentrations. Preeclampsia is frequently related to generation of small for gestational age (SGA) infant especially in cases with severe preeclampsia. However, it is still controversial whether the increase in maternal plasma leptin levels is associated with fetal growth restriction without complication of preeclampsia. Therefore, the aim of the present study was to explore the relationship between maternal plasma leptin levels and fetal growth in non-preeclamptic (n = 98) and preeclamptic (n = 40) women. In non-preeclamptic pregnant women, plasma leptin levels in SGA group (n = 11) were significantly higher than those in appropriate for gestational age (AGA) group (n = 87, P<0.05). In pregnant women with preeclampsia, likewise, plasma leptin levels in SGA group (n = 15) were significantly higher than those in AGA group (n = 25, P<0.05). In multiple linear regression analysis, maternal BMI, mean arterial blood pressure and ∆SD of neonatal body weight were significant factors for determining maternal plasma leptin levels in all population studied. Maternal BMI and ∆SD of neonatal body weight showed positive correlation with maternal plasma leptin levels when analysis was performed in non-preeclamptic subjects alone. In conclusion, maternal plasma leptin levels reflect, at least partly, deterioration in fetal growth.

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Section: Discussionsupporting

confidence: 93%

The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

et al. 2007

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“…23 Placental dysfunction has been suggested as a unifying mechanism underlying both fetal growth restriction and elevated maternal leptin levels (through increased placental production of leptin), al though this model remains speculative. 24 Like leptin, C-reactive protein also emerged as a negative determinant of infant birth weight in our multiple linear regression analysis. In the Hyperglycemia and Adverse Pregnancy Outcome Study, an inverse relation between C-reactive pro- tein level and birth weight was seen after adjustment for covariates, including maternal BMI.…”

Section: Discussionmentioning

confidence: 79%

“…An inverse relation between leptin level and infant birth weight has been observed in some, though not all, previous studies. [21][22][23][24] Of note, Verhaeghe and colleagues found that, compared with glucose, insulin, adiponectin and tumour necrosis factor-α, leptin was the mediator that was most strongly (and negatively) associated with birth weight. 23 Placental dysfunction has been suggested as a unifying mechanism underlying both fetal growth restriction and elevated maternal leptin levels (through increased placental production of leptin), al though this model remains speculative.…”

Section: Discussionmentioning

confidence: 99%

Effect of maternal weight, adipokines, glucose intolerance and lipids on infant birth weight among women without gestational diabetes mellitus

Retnakaran

Hanley

et al. 2012

CMAJ

116

110

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“…Leptin and adiponectin levels are dysregulated in pathological conditions such as GDM, pre-eclampsia and intrauterine growth restriction, representing an effect or a cause of disturbances in the feto/placento/maternal unit (Festa et al 1999, Lepercq et al 2001, Chan et al 2003, Pighetti et al 2003, Ranheim et al 2004, Williams et al 2004. Furthermore, a variety of hormones, cytokines and inflammatory stimuli have also been shown to regulate leptin, resistin and adiponectin expression and release.…”

Section: Introductionmentioning

confidence: 99%

Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies

Lappas

Yee²,

Permezel³

et al. 2005

Journal of Endocrinology

228

184

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The aim of this study was to determine the release and regulation of leptin, resistin and adiponectin from human placenta and fetal membranes, and maternal subcutaneous adipose tissue and skeletal muscle obtained from normal and gestational diabetes mellitus (GDM)-complicated pregnancies at the time of Cesarean section. Tissue explants were incubated in the absence (basal control) or presence of 10 µg/ml lipopolysaccharide (LPS), 10, 20 or 40 ng/ml tumor necrosis factor-(TNF-), interleukin (IL)-6 and IL-8, 1 µM phorbol myristate acetate, 10, 20 and 40 mM glucose, 0·1, 1 and 10 µM insulin and 0·1 1 and 10 µM dexamethasone, progesterone and estrogen. After an 18-h incubation, the medium was collected and the release of leptin, resistin and adiponectin was quantified by ELISA. Human gestational tissues and maternal tissues released immunoreactive leptin, resistin and adiponectin; however, there was no difference in the release of either resistin or adiponectin between normal pregnant women and women with gestational diabetes. The release of leptin was significantly higher in placenta, amnion and choriodecidua obtained from normal pregnant women compared with women with GDM. However, in maternal tissues, the situation was reversed, with adipose tissue and skeletal muscle obtained from women with GDM releasing significantly greater amounts of leptin. In adipose tissue and skeletal muscle the release of leptin was significantly greater in insulin-controlled GDM compared with diet-controlled GDM, and leptin release from adipose tissue was significantly correlated with maternal body mass index. In all tissues tested, there was no effect of incubation with LPS, IL-6, IL-8 or TNF-on leptin, resistin or adiponectin release. PMA significantly increased the release of resistin from placenta and adipose tissue. Insulin increased placental resistin release, whereas the hormones dexamethasone, progesterone and estrogen significantly decreased placental resistin release. The data presented in this study demonstrate that dysregulation of leptin metabolism and/or function in the placenta may be implicated in the pathogenesis of GDM. Furthermore, resistin release is greatly affected by a variety of inflammatory mediators and hormones.

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Maternal Serum and Umbilical Cord Blood Leptin Concentrations With Fetal Growth Restriction

Cited by 20 publications

References 21 publications

The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

Effect of maternal weight, adipokines, glucose intolerance and lipids on infant birth weight among women without gestational diabetes mellitus

Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies

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