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

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  • معلومة اضافية
    • المصدر:
      Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: Basel, Switzerland : MDPI, [2000-
    • الموضوع:
      Diabetes, Gestational/*drug therapy ; Fatty Acids/*metabolism ; Hypoglycemic Agents/*therapeutic use ; Insulin/*therapeutic use ; Placenta/*drug effects; Adiposity/drug effects ; Cell Line ; Diabetes, Gestational/metabolism ; Fatty Acid Transport Proteins/metabolism ; Fatty Acid-Binding Proteins/metabolism ; Female ; Fetus/drug effects ; Fetus/metabolism ; Humans ; Lipase/metabolism ; Lipoprotein Lipase/metabolism ; Placenta/metabolism ; Pregnancy
    • نبذة مختصرة :
      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.
      Competing Interests: The authors declare no conflict of interest.
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    • Contributed Indexing:
      Keywords: fetal adiposity; gestational diabetes; insulin resistance; placental lipid transport
    • الرقم المعرف:
      0 (Fatty Acid Transport Proteins)
      0 (Fatty Acid-Binding Proteins)
      0 (Fatty Acids)
      0 (Hypoglycemic Agents)
      0 (Insulin)
      EC 3.1.1.3 (LIPG protein, human)
      EC 3.1.1.3 (Lipase)
      EC 3.1.1.34 (Lipoprotein Lipase)
    • الموضوع:
      Date Created: 20170608 Date Completed: 20171128 Latest Revision: 20181113
    • الموضوع:
      20250114
    • الرقم المعرف:
      PMC5486026
    • الرقم المعرف:
      10.3390/ijms18061203
    • الرقم المعرف:
      28587267