Maternal insulin therapy does not restore foetoplacental endothelial dysfunction in gestational diabetes mellitus

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dc.contributor.authorSubiabre, Mario
dc.contributor.authorSilva, Luis
dc.contributor.authorVillalobos-Labra, Roberto
dc.contributor.authorToledo, Fernando
dc.contributor.authorPaublo, Mario
dc.contributor.authorLopez, Marcia A.
dc.contributor.authorSalsoso, Rocio
dc.contributor.authorPardo, Fabian
dc.contributor.authorLeiva, Andrea
dc.contributor.authorSobrevia, Luis
dc.date.accessioned2025-01-23T21:24:59Z
dc.date.available2025-01-23T21:24:59Z
dc.date.issued2017
dc.description.abstractPregnant 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.
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.bbadis.2017.07.022
dc.identifier.eissn1879-260X
dc.identifier.issn0925-4439
dc.identifier.urihttps://doi.org/10.1016/j.bbadis.2017.07.022
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101319
dc.identifier.wosidWOS:000415779300026
dc.issue.numero11
dc.language.isoen
dc.pagina.final2998
dc.pagina.inicio2987
dc.revistaBiochimica et biophysica acta-molecular basis of disease
dc.rightsacceso restringido
dc.subjectDiabetes
dc.subjectInsulin therapy
dc.subjectEndothelium
dc.subjectArginine
dc.subjectNitric oxide
dc.subjectUmbilical vein
dc.subject.ods03 Good Health and Well-being
dc.subject.ods05 Gender Equality
dc.subject.odspa03 Salud y bienestar
dc.subject.odspa05 Igualdad de género
dc.titleMaternal insulin therapy does not restore foetoplacental endothelial dysfunction in gestational diabetes mellitus
dc.typeartículo
dc.volumen1863
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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