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Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects

There is little information available on the effect of Gestational diabetes mellitus (GDM) treatment (diet or insulin) on placental lipid carriers, which may influence fetal fat accretion. Insulin may activate placental insulin receptors protein kinase (AKT) and extracellular signal regulated kinase...

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Autores principales: Ruiz-Palacios, Maria, Prieto-Sánchez, Maria Teresa, Ruiz-Alcaraz, Antonio José, Blanco-Carnero, José Eliseo, Sanchez-Campillo, Maria, Parrilla, Juan José, Larqué, Elvira
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5486026/
https://www.ncbi.nlm.nih.gov/pubmed/28587267
http://dx.doi.org/10.3390/ijms18061203
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author Ruiz-Palacios, Maria
Prieto-Sánchez, Maria Teresa
Ruiz-Alcaraz, Antonio José
Blanco-Carnero, José Eliseo
Sanchez-Campillo, Maria
Parrilla, Juan José
Larqué, Elvira
author_facet Ruiz-Palacios, Maria
Prieto-Sánchez, Maria Teresa
Ruiz-Alcaraz, Antonio José
Blanco-Carnero, José Eliseo
Sanchez-Campillo, Maria
Parrilla, Juan José
Larqué, Elvira
author_sort Ruiz-Palacios, Maria
collection PubMed
description There is little information available on the effect of Gestational diabetes mellitus (GDM) treatment (diet or insulin) on placental lipid carriers, which may influence fetal fat accretion. Insulin may activate placental insulin receptors protein kinase (AKT) and extracellular signal regulated kinase ERK mediators, which might affect lipid metabolism. Placenta was collected from 25 control women, 23 GDM-Diet and 20 GDM-Insulin. Western blotting of insulin signaling mediators and lipid carriers was performed. The human choricarcinoma-derived cell line BeWo was preincubated with insulin inhibitors protein kinase (AKT) and extracellular signal regulated kinase (ERK) and ERK inhibitors to evaluate insulin regulation of lipid carriers. Maternal serum insulin at recruitment correlated to ultrasound fetal abdominal circumference in offspring of GDM and placental endothelial lipase (EL). Lipoprotein lipase in placenta was significantly reduced in both GDM, while most of the other lipid carriers tended to higher values, although not significantly. There was a significant increase in both phosphorylated-Akt and ERK in placentas from GDM-Insulin patients; both were associated to placental fatty acid translocase (FAT), fatty acid binding protein (A-FABP), and EL. BeWo cells treated with insulin pathway inhibitors significantly reduced A-FABP, fatty acid transport protein (FATP-1), and EL levels, confirming the role of insulin on these carriers. We conclude that insulin promotes the phosphorylation of placental insulin mediators contributing to higher levels of some specific fatty acid carriers in the placenta and fetal adiposity in GDM.
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spelling pubmed-54860262017-06-29 Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects Ruiz-Palacios, Maria Prieto-Sánchez, Maria Teresa Ruiz-Alcaraz, Antonio José Blanco-Carnero, José Eliseo Sanchez-Campillo, Maria Parrilla, Juan José Larqué, Elvira Int J Mol Sci Article There is little information available on the effect of Gestational diabetes mellitus (GDM) treatment (diet or insulin) on placental lipid carriers, which may influence fetal fat accretion. Insulin may activate placental insulin receptors protein kinase (AKT) and extracellular signal regulated kinase ERK mediators, which might affect lipid metabolism. Placenta was collected from 25 control women, 23 GDM-Diet and 20 GDM-Insulin. Western blotting of insulin signaling mediators and lipid carriers was performed. The human choricarcinoma-derived cell line BeWo was preincubated with insulin inhibitors protein kinase (AKT) and extracellular signal regulated kinase (ERK) and ERK inhibitors to evaluate insulin regulation of lipid carriers. Maternal serum insulin at recruitment correlated to ultrasound fetal abdominal circumference in offspring of GDM and placental endothelial lipase (EL). Lipoprotein lipase in placenta was significantly reduced in both GDM, while most of the other lipid carriers tended to higher values, although not significantly. There was a significant increase in both phosphorylated-Akt and ERK in placentas from GDM-Insulin patients; both were associated to placental fatty acid translocase (FAT), fatty acid binding protein (A-FABP), and EL. BeWo cells treated with insulin pathway inhibitors significantly reduced A-FABP, fatty acid transport protein (FATP-1), and EL levels, confirming the role of insulin on these carriers. We conclude that insulin promotes the phosphorylation of placental insulin mediators contributing to higher levels of some specific fatty acid carriers in the placenta and fetal adiposity in GDM. MDPI 2017-06-06 /pmc/articles/PMC5486026/ /pubmed/28587267 http://dx.doi.org/10.3390/ijms18061203 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Ruiz-Palacios, Maria
Prieto-Sánchez, Maria Teresa
Ruiz-Alcaraz, Antonio José
Blanco-Carnero, José Eliseo
Sanchez-Campillo, Maria
Parrilla, Juan José
Larqué, Elvira
Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects
title Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects
title_full Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects
title_fullStr Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects
title_full_unstemmed Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects
title_short Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects
title_sort insulin treatment may alter fatty acid carriers in placentas from gestational diabetes subjects
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5486026/
https://www.ncbi.nlm.nih.gov/pubmed/28587267
http://dx.doi.org/10.3390/ijms18061203
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