Leptin Receptor in Human Term Placenta: in Situ Hybridization and Immunohistochemical Localization

Bodner, Johannes; Ebenbichler, Christoph; Wolf, Hans; Müller‐Holzner, Elisabeth; Stanzl, Ursula; Gander, R.; Huter, O.; Patsch, Josef R.

doi:10.1053/plac.1999.0431

Cited by 77 publications

(42 citation statements)

References 33 publications

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“…The placenta expresses receptors for numerous hormones including glucocorticoids, insulin, insulin-like growth factors (IGFs), leptin, gonadal hormones, cytokines, and prostaglandins (Bodner et al, 1999;Fowden et al, 2014;Hiden et al, 2006;Keelan and Mitchell, 2007;McCormick et al, 1981;Unlugedik et al, 2010). These signals are integrated by downstream cascades that ultimately influence placental growth, energy homeostasis, and endocrine action.…”

Section: Signal Detection and Response Coordinationmentioning

confidence: 99%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

205

180

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Adversity experienced during gestation is a predictor of lifetime neuropsychiatric disease susceptibility. Specifically, maternal stress during pregnancy predisposes offspring to sex-biased neurodevelopmental disorders, including schizophrenia, attention deficit/hyperactivity disorder, and autism spectrum disorders. Animal models have demonstrated disease-relevant endophenotypes in prenatally stressed offspring and have provided unique insight into potential programmatic mechanisms. The placenta has a critical role in the deleterious and sex-specific effects of maternal stress and other fetal exposures on the developing brain. Stress-induced perturbations of the maternal milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible for maintaining intrauterine homeostasis. Disruption of vital placental functions can have a significant impact on fetal development, including the brain, outcomes that are largely sex-specific. Here we review the novel involvement of the placenta in the transmission of the maternal adverse environment and effects on the developing brain.

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Section: Signal Detection and Response Coordinationmentioning

confidence: 99%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

205

180

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“…Human leptin mRNA and protein are also localized to the villous vascular endothelial cells, which are in direct contact with the fetal blood . Both long and short leptin receptor (Ob-R) isoforms are present in placenta, and are co-localized with leptin to the syncytiotrophoblast at the maternal interface (Bodner et al 1999, implicating a potential autocrine or paracrine effect of leptin on placental function.…”

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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“…The relative contribution of adipose and placental-derived leptin to circulating levels in the rodent is uncertain. The placenta has been shown to express both the leptin and leptin receptor genes (Hoggard et al 1997, Masuzaki et al 1997, Henson et al 1998, Bodner et al 1999. Interestingly, in humans, placental leptin expression in growthrestricted pregnancies is lower when compared with diabetic pregnancies and, relative to controls, the growthrestricted pregnancies have lower placental and cord blood leptin concentrations .…”

Section: Introductionmentioning

confidence: 99%

Circulating leptin during ovine pregnancy in relation to maternal nutrition, body composition and pregnancy outcome

Thomas¹,

Wallace²,

Aitken³

et al. 2001

Journal of Endocrinology

112

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This study examined the pattern of circulating leptin in age-matched sheep during adolescent pregnancy, and its relationship with maternal dietary intake, body composition and tissue expression of the leptin gene. Overfeeding the adolescent pregnant ewe results in rapid maternal growth at the expense of the placenta, leading to growth restriction in the fetus, compared with normal fed controls.Our results demonstrate that, in the adolescent ewe, overfeeding throughout pregnancy was associated with higher maternal leptin concentrations, when compared with moderately fed controls (P<0·05), with no peak in circulating leptin towards the end of pregnancy. There was a close correlation between indices of body composition and circulating leptin levels at day 104 of gestation and at term (P<0·03). Further, when the dietary intake was switched from moderate to high, or high to moderate, at day 50 of gestation, circulating leptin levels changed rapidly, in parallel with the changes in dietary intake. Leptin mRNA levels and leptin protein in perirenal adipose tissue samples, taken at day 128 of gestation, were higher in overfed dams (P<0·04), suggesting that adipose tissue was the source of the increase in circulating leptin in the overnourished ewes. Leptin protein was also detected in placenta but leptin gene expression was negligible. However, leptin receptor gene expression was detected in the ovine placenta, suggesting that the placenta is a target organ for leptin. A negative association existed between maternal circulating leptin and fetal birth weight, placental/cotyledon weight and cotyledon number.In conclusion, in this particular ovine model, hyperleptinaemia was not observed during late pregnancy. Instead, circulating leptin concentrations reflected increased levels of leptin secretion by adipose tissue primarily as a result of the increase in body fat deposition, due to overfeeding. However, there appears to be a direct effect of overfeeding, particularly in the short term. In the nutritional switch-over study, circulating leptin concentrations changed within 48 h of the change in dietary intake. The presence of leptin protein and leptin receptor gene expression in the placenta suggests that leptin could be involved in nutrient partitioning during placental and/or fetal development.

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Leptin Receptor in Human Term Placenta: in Situ Hybridization and Immunohistochemical Localization

Cited by 77 publications

References 33 publications

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

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

Circulating leptin during ovine pregnancy in relation to maternal nutrition, body composition and pregnancy outcome

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