Impact of Gestational Diabetes Mellitus in the Maternal-to-Fetal Transport of Nutrients

Araújo, João Pedro; Keating, Elisa; Martel, Fátima

doi:10.1007/s11892-014-0569-y

Cited by 53 publications

(34 citation statements)

References 96 publications

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“…Many studies point at a cross regulation of insulin pathways [33], which further hinders our understanding of the molecular mechanisms of this hormone. In addition, insulin is not the only molecule able to activate these signaling pathways, since cytokines, as well as other hormones and growth factors, play a very important role in their activation [9,31,33]. These molecules are also involved in cellular metabolism and may also affect the transport of nutrients.…”

Section: Placental Insulin Signaling Cascadementioning

confidence: 99%

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Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Ruiz-Palacios

Ruiz–Alcaraz²,

Sánchez-Campillo³

et al. 2017

Ann Nutr Metab

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Background: Gestational diabetes mellitus (GDM) is associated with increased fetal adiposity, which may increase the risk of obesity in adulthood. The placenta has insulin receptors and maternal insulin can activate its signaling pathways, affecting the transport of nutrients to the fetus. However, the effects of diet or insulin treatment on the placental pathophysiology of GDM are unknown. Summary: There are very few studies on possible defects in the insulin signaling pathway in the GDM placenta. Such defects could influence the placental transport of nutrients to the fetus. In this review we discuss the state of insulin signaling pathways in placentas of women with GDM, as well as the role of exogenous insulin in placental nutrient transport to the fetus, and fetal adiposity. Key Messages: Maternal insulin in the third trimester is correlated with fetal abdominal circumference at that time, suggesting the important role of insulin in this process. Since treatment with insulin at the end of pregnancy may activate placental nutrient transport to the fetus and promote placental fatty acid transfer, it would be interesting to improve maternal hyperlipidemia control in GDM subjects treated with this hormone. More research in this area with high number of subjects is necessary.

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Section: Placental Insulin Signaling Cascadementioning

confidence: 99%

“…Gestational diabetes changes the placental structure, which may alter the transport of nutrients to the fetus [9,10,11]. Maternal insulin is not required for the placental transfer of glucose, since this occurs mainly via GLUT-1, which is a carrier that acts independently of insulin.…”

Section: Introductionmentioning

confidence: 99%

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Ruiz-Palacios

Ruiz–Alcaraz²,

Sánchez-Campillo³

et al. 2017

Ann Nutr Metab

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“…This includes the establishment of physiological insulin resistance to form a glucose gradient across the placenta (30, 31). Gestational diabetes mellitus (GDM) occurs if the mother cannot adapt to this insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

Human Placental Hofbauer Cells Maintain an Anti-inflammatory M2 Phenotype despite the Presence of Gestational Diabetes Mellitus

et al. 2017

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BackgroundHofbauer cells (HBCs) are macrophages of the feto-placental unit. Despite the general view that these cells have an anti-inflammatory M2 phenotype, recent studies have claimed that pregnancy pathologies—e.g., gestational diabetes mellitus (GDM)—cause a switch from an M2 to an M1 pro-inflammatory phenotype in HBCs. The pilot-study presented here challenges this claim, showing that HBCs maintain anti-inflammatory properties in spite of the hyperglycemic, low-grade inflammatory environment of GDM.MethodsHBCs were isolated from placentae of healthy women (N = 5) and women with GDM (N = 6) diagnosed in the second trimester. FACS was used to measure surface markers associated with either M1 or M2 phenotype on the cells. In addition, placental tissue sections were subjected to immune histochemical imaging to assess the phenotype within the tissue context. Supernatant from control and GDM HBCs was collected at defined time points and used in a multiplex ELISA-on-beads approach to assess secretion of cytokines, chemokines, and growth factors. The effect of HBC cell culture supernatant on placental endothelial activation was investigated.ResultsFACS and immune staining showed that, indeed, M2 markers, such as CD206 and CD209, are increased in HBCs isolated from GDM placentae. Also, the M1 marker CD86 was increased, but only by trend. Secretion of numerous cytokines, chemokines and growth factors was not changed; pro-inflammatory interleukin (IL)-1β and IL-6 release form GDM HBC was increased but not significant. Exposure to GDM HBC supernatant did not induce cell adhesion molecules (VCAM-1, selectins, vascular endothelial-cadherin) in placental endothelial cells compared to supernatant from control HBCs, an induction of intracellular adhesion molecule 1 was observed however.ConclusionOur study—although performed in a small set of patients—shows that placental macrophages maintain their anti-inflammatory, tissue remodeling M2 phenotype even in pregnancies affected by gestational diabetes. This consistent phenotype might be important for propagation of maternal tolerance toward the fetus and for protection of the fetus from a low-grade inflammatory environment.

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“…Une synthèse accrue de collagène dans le mésenchyme placentaire ainsi que cellules bêta, affecte la production d'insuline. Des complications péri-natales, en particulier une macrosomie foetale, augmentent les risques obstétricaux liés à cette pathologie [26]. De plus, la présence d'un diabète gestationnel accroît le risque pour la descendance de développer des maladies cardiovasculaires et métaboliques ainsi que des dysfonctionnements cognitifs [27] (➜).…”

Section: Obésité Et Transferts Placentairesunclassified

“…Les transcrits codant les isoformes FABP (fatty acid binding protein) 4 et FABP5, protéines de liaison des acides gras, sont également surexprimés dans les placentas des patientes ayant un DT2 et un diabète gestationnel [43]. Dans ces derniers, le transfert placentaire des acides gras polyinsaturés à longues chaînes est perturbé [26]. Une surexpression des transporteurs des acides gras placentaires (FABP1, FABP3, FABP4 et ACSL [acyl-CoA synthethase long chain] 2, ACSL3 et ACSL4) a également été maternal environment, this organ is sensitive to metabolic disorders as over-nutrition, obesity or diabetes.…”

Section: Diabète Et Transfert Des Nutrimentsunclassified

Impact de l’obésité et du diabète maternels sur la fonction placentaire

et al. 2016

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> Situé à l'interface foeto-maternelle, le placenta exerce des fonctions d'échanges, endocrines et immunitaires qui influencent le développement foetal. En contact direct avec l'environnement maternel, cet organe est sensible aux désordres métaboliques comme la surnutrition, l'obésité ou le diabète. L'altération des paramètres sanguins associée à ces conditions affecte l'histologie, la vascularisation et les transferts des nutriments placentaires et induit, en fonction du trouble métabolique, une inflammation locale ou une hypoxie. Ces modifications placentaires perturbent le développement et la croissance foetale, ce qui augmente le risque de pathologies à l'âge adulte chez la descendance. Le placenta est donc un acteur incontournable de la programmation foetale. < cet environnement afin d'optimiser le transport des nutriments et des gaz et ainsi promouvoir la survie foetale. Les modifications phénotypiques du placenta ayant des effets sur le phénotype de l'individu, le placenta représente donc un acteur crucial de la programmation foetale ou DOHaD (developmental origins of health and disease), concept développé dans ce numéro thématique de médecine/sciences qui lui est consacré [4]. Dans cette synthèse, nous présenterons notamment l'impact des désordres métaboliques maternels, tels que l'obésité et le diabète, sur la fonction placentaire en nous appuyant sur des données obtenues chez l'homme et à partir de modèles animaux. Effets de l'obésité sur la fonction placentaireLa prévalence de l'obésité ne cesse d'augmenter dans le monde. En France, d'après l'enquête ObEpi-Roche publiée en 2012 1 , une femme sur cinq en âge de procréer est en surpoids, et environ 15 % des femmes présentent une obésité (index de masse corporelle, IMC ≥ 30 kg/m 2 ). Cette obésité pré-gestationnelle favorise, au cours de la grossesse, les anomalies de la croissance foetale, le développement d'un diabète gestationnel, le retard de croissance intra-utérin (RCIU) ou la macrosomie, la pré-éclampsie et la mortalité foetale (➜).1

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Impact of Gestational Diabetes Mellitus in the Maternal-to-Fetal Transport of Nutrients

Cited by 53 publications

References 96 publications

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Human Placental Hofbauer Cells Maintain an Anti-inflammatory M2 Phenotype despite the Presence of Gestational Diabetes Mellitus

Impact de l’obésité et du diabète maternels sur la fonction placentaire

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