Hyperinsulinemia Increases Placenta Endothelin-Converting Enzyme-1 Expression in Trophoblasts

Khamaisi, Mogher; Skarzinski, Galina; Mekler, Judith; Zreik, Farid; Damouni, Rawan; Ariel, Ilana; Bursztyn, Michael

doi:10.1038/ajh.2011.164

Cited by 12 publications

(3 citation statements)

References 26 publications

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“…Bursztyn's group performed a series of studies to evaluate the effects of chronic hyperinsulinemia during gestation. 15,16,[26][27][28] As expected, they observed that pregnant rats treated with insulin 1 week before and throughout pregnancy by subcutaneously implanted sustained-release insulin pellets had elevated serum insulin levels (approximately 78%) compared with normal pregnant rats. 15 They showed that systolic blood pressure measured by tail cuff was increased in insulin-treated pregnant rats on GD 19 and 20.…”

Section: Discussionsupporting

confidence: 60%

Euglycemic Hyperinsulinemia Increases Blood Pressure in Pregnant Rats Independent of Placental Antiangiogenic and Inflammatory Factors

Palei

Spradley²,

Granger³

2013

American Journal of Hypertension

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Section: Discussionsupporting

confidence: 60%

Euglycemic Hyperinsulinemia Increases Blood Pressure in Pregnant Rats Independent of Placental Antiangiogenic and Inflammatory Factors

Palei

Spradley²,

Granger³

2013

American Journal of Hypertension

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“…Subsequent studies in this model showed that insulin reduced PlGF and arrested trophoblast invasion in the uterus (168). Intriguingly, it was noted that the trophoblasts in placentas from the hyperinsulinemic rats expressed greater endothelin converting enzyme (82). The major cleavage product of this enzyme is ET-1.…”

Section: Effects Of Obesity On the Placental Function And Perfusionmentioning

confidence: 96%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

115

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) is a pregnancy-specific disorder typically presenting as new-onset hypertension and proteinuria. While numerous epidemiological studies have demonstrated that obesity increases the risk of PE, the mechanisms have yet to be fully elucidated. Growing evidence from animal and human studies implicate placental ischemia in the etiology of this maternal syndrome. It is thought that placental ischemia is brought about by dysfunctional cytotrophoblast migration and invasion into the uterus and subsequent lack of spiral arteriole widening and placental perfusion. Placental ischemia/ hypoxia stimulates the release of soluble placental factors into the maternal circulation where they cause endothelial dysfunction, particularly in the kidney, to elicit the clinical manifestations of PE. The most recognized of these factors are the anti-angiogenic sFlt-1 and pro-inflammatory TNF-␣ and AT1-AA, which promote endothelial dysfunction by reducing levels of the provasodilator nitric oxide and stimulating production of the potent vasoconstrictor endothelin-1 and reactive oxygen species. We hypothesize that obesity-related metabolic factors increase the risk for developing PE by impacting various stages in the pathogenesis of PE, namely, 1) cytotrophoblast migration and placental ischemia; 2) release of soluble placental factors into the maternal circulation; and 3) maternal endothelial and vascular dysfunction. This review will summarize the current experimental evidence supporting the concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors. body mass index; inflammation; placental ischemia; pregnancy; RUPP; sFlt-1 PE IS A PREGNANCY-SPECIFIC DISORDER typically identified by new-onset hypertension in the second half of pregnancy. Although often accompanied by new-onset proteinuria, PE can be associated with many other signs and symptoms including headaches, visual disturbances, epigastric pain, and the development of edema (4,192). Globally, this disease affects over 8 million pregnancies per year and is estimated to account for 40 -60% of maternal deaths in developing countries (125). In the United States, there was a 25% increase in the rate of PE between the years 1987-2004 (189). This significant increase highlights the importance of understanding how risk factors like obesity play a role in the pathogenesis of this maternal syndrome. Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Greater than one-half of pregnant women are overweight or obese (48), and more than two-thirds of reproductive-aged women in the United States are overweight or obese (49). Although mounting epidemiological evidence supports obesity as a major risk factor for PE, the mechanisms linking these two morbidities are...

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“…Sabe-se que os fatores circulantes maternos, como nutrientes, metabólitos e hormônios apresentam papel fundamental durante a gestação pois, dentre outras funções, regulam o desenvolvimento da placenta. Os níveis de insulina séricos maternos, por exemplo, apesar de não atravessarem a barreira placentária para que possam exercer alguma função direta nos órgãos fetais, quando em altas concentrações, podem alterar a função placentária (150)(151)(152).…”

Section: A Prole De Mães Resistentes E Propensas à Obesidade Apresent...unclassified

Modulação de Let-7 hepático e os efeitos na homeostasia energética em prole programada pela obesidade materna

Angélica de Paula Simino

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Hyperinsulinemia Increases Placenta Endothelin-Converting Enzyme-1 Expression in Trophoblasts

Abstract: ECE-1 and ET-A are expressed in the trophoblastic cells of the placenta and MT. This may affect local endothelin levels, BP and IUGR.

Cited by 12 publications

References 26 publications

Euglycemic Hyperinsulinemia Increases Blood Pressure in Pregnant Rats Independent of Placental Antiangiogenic and Inflammatory Factors

Euglycemic Hyperinsulinemia Increases Blood Pressure in Pregnant Rats Independent of Placental Antiangiogenic and Inflammatory Factors

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Modulação de Let-7 hepático e os efeitos na homeostasia energética em prole programada pela obesidade materna

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