Placental metabolism and disease

Sobrevía, Luis

doi:10.1016/j.placenta.2018.09.001

Cited by 5 publications

(3 citation statements)

References 20 publications

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“…Altogether, the available evidence, even when limited, suggests that the sexual dimorphism in fat accumulation, fatty liver, and systemic insulin resistance could associate with a higher occurrence of ER stress in men compared with women. Unfortunately, whether ER stress is also under modulation by gender is still not described (Sobrevia, 2018;Subiabre et al, 2018;Villalobos-Labra et al, 2017).…”

Section: Gender-associated Insulin Resistance Predispositionmentioning

confidence: 99%

Endoplasmic reticulum stress and development of insulin resistance in adipose, skeletal, liver, and foetoplacental tissue in diabesity

Villalobos-Labra

Subiabre

Toledo

et al. 2019

Molecular Aspects of Medicine

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Diabesity is an abnormal metabolic condition shown by patients with obesity that develop type 2 diabetes mellitus. Patients with diabesity present with insulin resistance, reduced vascular response to insulin, and vascular endothelial dysfunction. Along with the several well-described mechanisms of insulin resistance, a state of endoplasmic reticulum (ER) stress, where the primary human targets are the adipose tissue, liver, skeletal muscle, and the foetoplacental vasculature, is apparent. ER stress characterises by the activation of the unfolded protein response via three canonical ER stress sensors, i.e., the protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6. Slightly different cell signalling mechanisms preferentially enable in diabesity in the ER stress-associated insulin resistance for adipose tissue (IRE1α/X-box binding protein 1 mRNA splicing/c-jun N-terminal kinase 1 activation), skeletal muscle (tribbles-like protein 3 (TRB3)/proinflammatory cytokines activation), and liver (PERK/activating transcription factor 4/TRB3 activation). There is no information in human subjects with diabesity in the foetoplacental vasculature. However, the available literature shows that pregnant women with pre-pregnancy obesity or overweight that develop gestational diabetes mellitus (GDM) and their newborn show insulin resistance. ER stress is recently reported to be triggered in endothelial cells from the human umbilical vein from mothers with pre-pregnancy obesity. However, whether a different metabolic alteration to obesity in pregnancy or GDM is present in women with pre-pregnancy obesity that develop GDM, is unknown. In this review, we summarised the findings on diabesity-associated mechanisms of insulin resistance with emphasis in the primary targets adipose, skeletal muscle, liver, and foetoplacental tissues. We also give evidence on the possibility of a new GDM-associated metabolic condition triggered in pregnancy by maternal obesity, i.e. gestational diabesity, leading to ER stress-associated insulin resistance in the human foetoplacental vasculature.

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Section: Gender-associated Insulin Resistance Predispositionmentioning

confidence: 99%

Endoplasmic reticulum stress and development of insulin resistance in adipose, skeletal, liver, and foetoplacental tissue in diabesity

Villalobos-Labra

Subiabre

Toledo

et al. 2019

Molecular Aspects of Medicine

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“…During pregnancy, the placenta and the UC form vital temporary organs to sustain proper fetal development. Therefore, any alteration in the in-utero condition is directly or secondarily associated with the placental or UC disorders, like intrauterine hypoxia and an impaired blood flow to the fetus [72][73][74] . Moreover a recently published chemo-biology interactome analysis underlined this concept and provided evidence that components of tobacco smoke intensively influence gene expression at both embryonic and fetal developmental period 96 .…”

Section: Discussionmentioning

confidence: 99%

“…A terhesség során olyan átmeneti szervek biztosítják a magzati fejlődést, mint a méhlepény és a köldökzsinór. Ezért a méhen belüli állapotok megváltozása közvetlenül vagy közvetett módon kapcsolódnak a placenta vagy a köldökzsinór olyan rendellenességeihez, mint az intrauterin hypoxia és az elégtelen magzati vérellátás [72][73][74] . Emellett egy nemrégiben publikált kemo-biológiai interaktóm analízis megerősítette, és bizonyítékot szolgáltatott arra, hogy a dohányfüst komponensei intenzíven befolyásolják a génexpressziót mind embrionális, mind pedig a magzati fejlődési időszakban 96 Az eredmények így azt valószínűsítik, hogy a VVT-k NOS3-függő NO termelése nem érvényesülhet kompenzációs mechanizmusként 251,253,254 .…”

Section: öSszefoglalásunclassified

A terhesség alatti dohányzással összefüggésbe hozható endotéliális diszfunkció molekuláris vizsgálata köldökzsinór modellrendszerben

Zahorán

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Fetoplacental vasculature as a model to study human cardiovascular endocrine disruption

Lorigo

2022

Molecular Aspects of Medicine

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Placental metabolism and disease

Cited by 5 publications

References 20 publications

Endoplasmic reticulum stress and development of insulin resistance in adipose, skeletal, liver, and foetoplacental tissue in diabesity

Endoplasmic reticulum stress and development of insulin resistance in adipose, skeletal, liver, and foetoplacental tissue in diabesity

A terhesség alatti dohányzással összefüggésbe hozható endotéliális diszfunkció molekuláris vizsgálata köldökzsinór modellrendszerben

Fetoplacental vasculature as a model to study human cardiovascular endocrine disruption

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