id paper:paper_00185043_v48_n1_p62_PerezPerez
record_format dspace
spelling 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