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  1. Home
  2. Browse by Author

Browsing by Author "Silva, Luis"

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    Foetoplacental epigenetic changes associated with maternal metabolic dysfunction
    (2018) Kerr, Bredford; Leiva Mendoza, Andrea Alejandra; Farías Jofré, Marcelo Enrique; Contreras Duarte, Susana de las Mercedes; Toledo, Fernando; Stolzenbach, Francisca; Silva, Luis; Sobrevía Luarte, Luis Alberto
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    Insulin therapy and its consequences for the mother, foetus, and newborn in gestational diabetes mellitus
    (2018) Subiabre Morales, Mario Enrique; Silva, Luis; Toledo, Fernando; Paublo, Mario; López, Marcia A.; Boric P., Mauricio; Sobrevía Luarte, Luis Alberto
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    Maternal insulin therapy does not restore foetoplacental endothelial dysfunction in gestational diabetes mellitus
    (2017) Subiabre, Mario; Silva, Luis; Villalobos-Labra, Roberto; Toledo, Fernando; Paublo, Mario; Lopez, Marcia A.; Salsoso, Rocio; Pardo, Fabian; Leiva, Andrea; Sobrevia, Luis
    Pregnant women diagnosed with gestational diabetes mellitus subjected to diet (GDMd) that do not reach normal glycaemia are passed to insulin therapy (GDMi). GDMd associates with increased human cationic amino acid transporter 1 (hCAT-1)-mediated transport of L-arginine and nitric oxide synthase (NOS) activity in foetoplacental vasculature, a phenomenon reversed by exogenous insulin. Whether insulin therapy results in reversal of the GDMd effect on the foetoplacental vasculature is unknown. We assayed whether insulin therapy normalizes GDMd-associated foetoplacental endothelial dysfunction. Primary cultures of human umbilical vein endothelial cells (HUVECs) from GDMi pregnancies were used to assay L-arginine transport kinetics, NOS activity, p44/42(mapk) and protein kinase B/Akt activation, and umbilical vein rings reactivity. HUVECs from GDMi or GDMd show increased hCAT-1 expression and maximal transport capacity, NOS activity, and eNOS, and p44/42(mapk), but not Akt activator phosphorylation. Dilation in response to insulin or calcitonin-gene related peptide was impaired in umbilical vein rings from GDMi and GDMd pregnancies. Incubation of HUVECs in vitro with insulin (1 nmol/L) restored hCAT-1 and eNOS expression and activity, and eNOS and p44/42(mapk) activator phosphorylation. Thus, maternal insulin therapy does not seem to reverse GDMd-associated alterations in human foetoplacental vasculature.

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