Pregestational diabetes increases fetoplacental vascular resistance in rats

Vajnerová, Olga; Kafka, P; Kratzerova, Tereza; Chalupský, Karel; Hampl, Václav

doi:10.1016/j.placenta.2018.01.008

Cited by 5 publications

(1 citation statement)

References 53 publications

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“…Combined with the unbalanced OS system and significantly decreased AMPKα phosphorylation, it is rational to detect an increased glycolytic rate and GLUT1 level under hyperglycemic conditions. It is worth noting that women with more advanced PGDM were likely to have severe underlying vascular diseases and abnormal placenta morphology, which may result in limited vascular resistance and nutrient availability [ 46 , 47 ]. Further experiments designed to differentiate the metabolic status of STB and CTB, respectively, were also needed.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia in Pregnancy-Associated Oxidative Stress Augments Altered Placental Glucose Transporter 1 Trafficking via AMPKα/p38MAPK Signaling Cascade

Wang

Ning

Huai

et al. 2022

IJMS

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GLUT1, being a ubiquitous transporter isoform, is considered primarily responsible for glucose uptake during glycolysis. However, there is still uncertainty about the regulatory mechanisms of GLUT1 in hyperglycemia in pregnancy (HIP, PGDM, and GDM) accompanied by abnormal oxidative stress responses. In the present study, it was observed that the glycolysis was enhanced in GDM and PGDM pregnancies. In line with this, the antioxidant system was disturbed and GLUT1 expression was increased due to diabetes impairment in both placental tissues and in vitro BeWo cells. GLUT1 responded to high glucose stimulation through p38MAPK in an AMPKα-dependent manner. Both the medical-mediated and genetic depletion of p38MAPK in BeWo cells could suppress GLUT1 expression and OS-induced proapoptotic effects. Furthermore, blocking AMPKα with an inhibitor or siRNA strategy promoted p38MAPK, GLUT1, and proapoptotic molecules expression and vice versa. In general, a new GLUT1 regulation pathway was identified, which could exert effects on placental transport function through the AMPKα-p38MAPK pathway. AMPKα may be a therapeutic target in HIP for alleviating diabetes insults.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia in Pregnancy-Associated Oxidative Stress Augments Altered Placental Glucose Transporter 1 Trafficking via AMPKα/p38MAPK Signaling Cascade

Wang

Ning

Huai

et al. 2022

IJMS

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Placental hypoxia: What have we learnt from small animal models?

Siragher

Sferruzzi‐Perri

2021

Placenta

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The role of microRNAs in pregnancies complicated by maternal diabetes

Owen,

Kennedy,

Quilang

et al. 2024

Clinical Science

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With the global prevalence of diabetes increasing, more people of reproductive age are experiencing hyperglycaemic pregnancies. Maternal Type 1 (T1DM) or Type 2 (T2DM) diabetes mellitus, and gestational diabetes mellitus (GDM) are associated with maternal cardiovascular and metabolic complications. Pregnancies complicated by maternal diabetes also increase the risk of short- and long-term health complications for the offspring, including altered fetal growth and the onset of T2DM and cardiometabolic diseases throughout life. Despite advanced methods for improving maternal glucose control, the prevalence of adverse maternal and offspring outcomes associated with maternal diabetes remains high. The placenta is a key organ at the maternal–fetal interface that regulates fetal growth and development. In pregnancies complicated by maternal diabetes, altered placental development and function has been linked to adverse outcomes in both mother and fetus. Emerging evidence suggests that microRNAs (miRNAs) are key molecules involved in mediating these changes. In this review, we describe the role of miRNAs in normal pregnancy and discuss how miRNA dysregulation in the placenta and maternal circulation is associated with suboptimal placental development and pregnancy outcomes in individuals with maternal diabetes. We also discuss evidence demonstrating that miRNA dysregulation may affect the long-term health of mothers and their offspring. As such, miRNAs are potential candidates as biomarkers and therapeutic targets in diabetic pregnancies at risk of adverse outcomes.

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Pregestational diabetes increases fetoplacental vascular resistance in rats

Cited by 5 publications

References 53 publications

Hyperglycemia in Pregnancy-Associated Oxidative Stress Augments Altered Placental Glucose Transporter 1 Trafficking via AMPKα/p38MAPK Signaling Cascade

Hyperglycemia in Pregnancy-Associated Oxidative Stress Augments Altered Placental Glucose Transporter 1 Trafficking via AMPKα/p38MAPK Signaling Cascade

Placental hypoxia: What have we learnt from small animal models?

The role of microRNAs in pregnancies complicated by maternal diabetes

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