Hyperinsulinemia Stimulates Angiogenesis of Human Fetoplacental Endothelial Cells: A Possible Role of Insulin in Placental Hypervascularization in Diabetes Mellitus

Lassance, Luciana; Miedl, Heidi; Absenger, Markus; Díaz-Pérez, Francisca; Lang, Uwe; Desoyé, Gernot; Hiden, Ursula

doi:10.1210/jc.2013-1210

Cited by 63 publications

(41 citation statements)

References 45 publications

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“…Acting through IGF-1 or hybrid IGF1/insulin receptors, insulin and/or IGF-1 could have a direct effect on adipose tissue endothelial cells. Indeed, the effects of insulin to stimulate endothelial cell proliferation (45,46) and VEGF production (47,48) have been reported and are consistent with our findings of activated receptors along the adipose tissue vasculature. Alternatively, insulin and IGF-1 could stimulate other cells in the tissue, including adipocytes, to produce pro-angiogenic factors.…”

Section: Discussionsupporting

confidence: 92%

Control of Adipose Tissue Expandability in Response to High Fat Diet by the Insulin-like Growth Factor-binding Protein-4

Gealekman

Gurav

Chouinard

et al. 2014

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 92%

Control of Adipose Tissue Expandability in Response to High Fat Diet by the Insulin-like Growth Factor-binding Protein-4

Gealekman

Gurav

Chouinard

et al. 2014

Journal of Biological Chemistry

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“…In mammals, insulin also mediates mitogenic effects in a variety of cell types (Stout, 1991; Qiao et al, 2005; Simó et al, 2006; Shrader et al, 2009; Heidegger et al, 2014). However, other reports have failed to find an insulin-mediated endothelial proliferative response (Liu et al, 2009; Lassance et al, 2013). …”

Section: Insulin and Insulin Receptorsmentioning

confidence: 93%

Pro-angiogenic Role of Insulin: From Physiology to Pathology

et al. 2017

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The underlying molecular mechanisms involve in the regulation of the angiogenic process by insulin are not well understood. In this review article, we aim to describe the role of insulin and insulin receptor activation on the control of angiogenesis and how these mechanisms can be deregulated in human diseases. Functional expression of insulin receptors and their signaling pathways has been described on endothelial cells and pericytes, both of the main cells involved in vessel formation and maturation. Consequently, insulin has been shown to regulate endothelial cell migration, proliferation, and in vitro tubular structure formation through binding to its receptors and activation of intracellular phosphorylation cascades. Furthermore, insulin-mediated pro-angiogenic state is potentiated by generation of vascular growth factors, such as the vascular endothelial growth factor, produced by endothelial cells. Additionally, diseases such as insulin resistance, obesity, diabetes, and cancer may be associated with the deregulation of insulin-mediated angiogenesis. Despite this knowledge, the underlying molecular mechanisms need to be elucidated in order to provide new insights into the role of insulin on angiogenesis.

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“…Moreover, insulin, along with glucose, is involved in the regulation of angiogenesis and vasculogenesis in the fetus [20,21], where they bind to fetal endothelial cells [22]. Thus, fetal hyperinsulinemia may also contribute to the hypervascular placenta typical of GDM [23]. Fetal insulin binds to the fetal endothelium IRs and alters the expression of several genes involved in signal transduction, metabolism, and transport [12].…”

Section: Functions Of Insulin Within the Placentamentioning

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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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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Hyperinsulinemia Stimulates Angiogenesis of Human Fetoplacental Endothelial Cells: A Possible Role of Insulin in Placental Hypervascularization in Diabetes Mellitus

Abstract: Elevated fetal insulin levels may contribute to the placental hypervascularization in diabetes via the phosphatidylinositol 3-kinase/Akt/eNOS pathway and involve Rac1. However, insulin does not stimulate proliferation and may need to cooperate with other growth factors.

Cited by 63 publications

References 45 publications

Control of Adipose Tissue Expandability in Response to High Fat Diet by the Insulin-like Growth Factor-binding Protein-4

Control of Adipose Tissue Expandability in Response to High Fat Diet by the Insulin-like Growth Factor-binding Protein-4

Pro-angiogenic Role of Insulin: From Physiology to Pathology

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

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