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Int. J. Mol. Sci. 2017, 18(6), 1203; doi:10.3390/ijms18061203

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

1
Department of Physiology, Faculty of Biology, Campus Mare Nostrum, University of Murcia, Murcia 30100, Spain
2
Obstetrics and Gynecology Service, Virgen de la Arrixaca Clinical Hospital, University of Murcia, Murcia 30120, Spain
3
Department of Biochemistry, Molecular Biology B and Immunology, Campus Mare Nostrum, University of Murcia, Murcia 30100, Spain
*
Author to whom correspondence should be addressed.
Academic Editor: Giovanni Tarantino
Received: 8 May 2017 / Revised: 31 May 2017 / Accepted: 2 June 2017 / Published: 6 June 2017
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
View Full-Text   |   Download PDF [1852 KB, uploaded 6 June 2017]   |  

Abstract

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. View Full-Text
Keywords: gestational diabetes; placental lipid transport; insulin resistance; fetal adiposity gestational diabetes; placental lipid transport; insulin resistance; fetal adiposity
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MDPI and ACS Style

Ruiz-Palacios, M.; Prieto-Sánchez, M.T.; Ruiz-Alcaraz, A.J.; Blanco-Carnero, J.E.; Sanchez-Campillo, M.; Parrilla, J.J.; Larqué, E. Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects. Int. J. Mol. Sci. 2017, 18, 1203.

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