Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects
Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found...
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paper:paper_00185043_v48_n1_p62_PerezPerez2023-06-08T14:39:34Z Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects Maymó, Julieta L. Varone, Cecilia Laura gestational diabetes insulin leptin placenta signal transduction insulin insulin receptor insulin receptor substrate IRS1 protein, human leptin leptin receptor adult biological model case control study dose response down regulation female human immunohistochemistry metabolism phosphorylation placenta pregnancy pregnancy diabetes mellitus signal transduction Adult Case-Control Studies Diabetes, Gestational Dose-Response Relationship, Drug Down-Regulation Female Humans Immunohistochemistry Insulin Insulin Receptor Substrate Proteins Leptin Models, Biological Phosphorylation Placenta Pregnancy Receptor, Insulin Receptors, Leptin Signal Transduction Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found in different cellular systems. Gestational diabetes (GDM) is a pathophysiological state with high circulating levels of both insulin and leptin. We have previously found that these 3 signaling pathways are activated in placenta from GDM patients to promote translation, involving the activation of leptin receptor. Now, we have tested the hypothesis that both leptin and insulin receptors might contribute to this activation in a positive way that may become negative when the system is overactivated. We studied the activation of leptin and insulin receptors in placenta from GDM and healthy pregnancies. We have also performed in vitro studies with insulin and leptin stimulation of trophoblast explants from healthy placenta. We have found that both leptin and insulin receptors are activated in placenta from GDM. In vitro stimulation of trophoblast explants with both leptin and insulin at submaximal doses (0.1 nM) potentiated the activation of signaling, whereas preincubation with maximal concentrations of insulin (10 nM) and further stimulation with leptin showed negative effect. Trophoblastic explants from GDM placenta, which presented high signaling levels, had a negative signaling effect when further incubated in vitro with leptin. In conclusion, insulin and leptin receptors have positive effects on signaling, contributing to high signaling levels in GDM placenta, but insulin and leptin have negative effects upon overstimulation. © Georg Thieme Verlag KG Stuttgart · New York. Fil:Maymó, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Varone, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2015 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00185043_v48_n1_p62_PerezPerez http://hdl.handle.net/20.500.12110/paper_00185043_v48_n1_p62_PerezPerez |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
gestational diabetes insulin leptin placenta signal transduction insulin insulin receptor insulin receptor substrate IRS1 protein, human leptin leptin receptor adult biological model case control study dose response down regulation female human immunohistochemistry metabolism phosphorylation placenta pregnancy pregnancy diabetes mellitus signal transduction Adult Case-Control Studies Diabetes, Gestational Dose-Response Relationship, Drug Down-Regulation Female Humans Immunohistochemistry Insulin Insulin Receptor Substrate Proteins Leptin Models, Biological Phosphorylation Placenta Pregnancy Receptor, Insulin Receptors, Leptin Signal Transduction |
spellingShingle |
gestational diabetes insulin leptin placenta signal transduction insulin insulin receptor insulin receptor substrate IRS1 protein, human leptin leptin receptor adult biological model case control study dose response down regulation female human immunohistochemistry metabolism phosphorylation placenta pregnancy pregnancy diabetes mellitus signal transduction Adult Case-Control Studies Diabetes, Gestational Dose-Response Relationship, Drug Down-Regulation Female Humans Immunohistochemistry Insulin Insulin Receptor Substrate Proteins Leptin Models, Biological Phosphorylation Placenta Pregnancy Receptor, Insulin Receptors, Leptin Signal Transduction Maymó, Julieta L. Varone, Cecilia Laura Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects |
topic_facet |
gestational diabetes insulin leptin placenta signal transduction insulin insulin receptor insulin receptor substrate IRS1 protein, human leptin leptin receptor adult biological model case control study dose response down regulation female human immunohistochemistry metabolism phosphorylation placenta pregnancy pregnancy diabetes mellitus signal transduction Adult Case-Control Studies Diabetes, Gestational Dose-Response Relationship, Drug Down-Regulation Female Humans Immunohistochemistry Insulin Insulin Receptor Substrate Proteins Leptin Models, Biological Phosphorylation Placenta Pregnancy Receptor, Insulin Receptors, Leptin Signal Transduction |
description |
Insulin and leptin receptors are known to share signaling pathways, such as JAK2/STAT-3 (Janus kinase2/signal transduction and activator of transcription3), MAPK (Mitogen activated protein kinase), and PI3K (phosphoinositide 3-kinase). Both positive and negative cross-talk have been previously found in different cellular systems. Gestational diabetes (GDM) is a pathophysiological state with high circulating levels of both insulin and leptin. We have previously found that these 3 signaling pathways are activated in placenta from GDM patients to promote translation, involving the activation of leptin receptor. Now, we have tested the hypothesis that both leptin and insulin receptors might contribute to this activation in a positive way that may become negative when the system is overactivated. We studied the activation of leptin and insulin receptors in placenta from GDM and healthy pregnancies. We have also performed in vitro studies with insulin and leptin stimulation of trophoblast explants from healthy placenta. We have found that both leptin and insulin receptors are activated in placenta from GDM. In vitro stimulation of trophoblast explants with both leptin and insulin at submaximal doses (0.1 nM) potentiated the activation of signaling, whereas preincubation with maximal concentrations of insulin (10 nM) and further stimulation with leptin showed negative effect. Trophoblastic explants from GDM placenta, which presented high signaling levels, had a negative signaling effect when further incubated in vitro with leptin. In conclusion, insulin and leptin receptors have positive effects on signaling, contributing to high signaling levels in GDM placenta, but insulin and leptin have negative effects upon overstimulation. © Georg Thieme Verlag KG Stuttgart · New York. |
author |
Maymó, Julieta L. Varone, Cecilia Laura |
author_facet |
Maymó, Julieta L. Varone, Cecilia Laura |
author_sort |
Maymó, Julieta L. |
title |
Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects |
title_short |
Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects |
title_full |
Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects |
title_fullStr |
Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects |
title_full_unstemmed |
Insulin and Leptin Signaling in Placenta from Gestational Diabetic Subjects |
title_sort |
insulin and leptin signaling in placenta from gestational diabetic subjects |
publishDate |
2015 |
url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00185043_v48_n1_p62_PerezPerez http://hdl.handle.net/20.500.12110/paper_00185043_v48_n1_p62_PerezPerez |
work_keys_str_mv |
AT maymojulietal insulinandleptinsignalinginplacentafromgestationaldiabeticsubjects AT varonececilialaura insulinandleptinsignalinginplacentafromgestationaldiabeticsubjects |
_version_ |
1768542017773633536 |