Endothelial dysfunction and reduced insulin response in umbilical vein from the offspring of maternal obesity pregnancies

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dc.catalogadorpau
dc.contributor.authorVillalobos Labra, Roberto Esteban
dc.contributor.authorPizarro, Carolina
dc.contributor.authorWestermeier Lafuente, Francisco David
dc.contributor.authorSáez Pedraza, Pablo José
dc.contributor.authorSobrevía Luarte, Luis Alberto
dc.contributor.authorFarías Jofré, Marcelo Enrique
dc.date.accessioned2023-05-18T19:49:47Z
dc.date.available2023-05-18T19:49:47Z
dc.date.issued2016
dc.description.abstractINTRODUCTION: Maternal obesity (MO) has been recognized as a risk factor for maternal and fetal complications, including offspring´s insulin resistance (IR) later in life. We evaluated the effect of MO in endothelial cells function and umbilical vein vasodilatation in response to insulin. METHODS: Primary cultures of human umbilical vein endothelial cells (HUVEC) and rings were isolated from normal (HUVEC-N) or MO (HUVEC-OB) pregnancies attending to Pontificia Universidad Católica de Chile Hospital. Total and/or phosphorylated level of IRS-1, Akt, MAPK and eNOS, were measured by western blot in protein extracts of cells exposed to insulin (1 nM, 30 min). Wire myography was used to evaluate functional effect of insulin in umbilical vein rings. Cellular nitric oxide (NO) availability was measured using the fluorescent probe diaminofluorescein (DAF). Values are Mean±S.E.M. RESULTS: MO was associated with inhibition of IRS-1 and reduced phosphorylation of Akt (2,24±0,06 vs 6,85±0,12; p<0,01) and MAPK (4,13±0,65 vs 13,12±1,67; p<0,01) in response to insulin, in HUVEC. We found that total eNOS and the activating phosphorylation on Ser1177 was reduced (0,98±0,03 vs 5,45±0,85; p<0,01) in HUVEC-OB compared to HUVEC-N. Conversely, the inhibitory phosphorylation on Thr495 was increased (1,88±0,08 vs 1,51±0,14; p<0,01) in HUVEC-OB. Also, HUVEC-N exposed to insulin (1nM) showed increased levels of NO at 5, 15 and 30 min of incubation, an effect blocked by the inhibitor of NOS L-NAME. In contrast, insulin did not increase NO production in HUVECOB. Finally, vein rings from MO showed abolished relaxation in response to insulin, meanwhile rings from normal pregnancies showed a 20% of insulin dilator effect, which was blocked by L-NAME. CONCLUSIONS: We have shown evidence that MO promotes less vasodilation of umbilical vein in response to insulin, due to an inhibitory state of insulin signaling and eNOS activation, with the consequent absence of insulin-dependent NO production by HUVEC affected by MO.
dc.format.extent1 página
dc.fuente.origenORCID
dc.identifier.doi10.1177/1933719116641257
dc.identifier.issn1933-7191
dc.identifier.urihttps://publons.com/wos-op/publon/18766661/
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/67120
dc.information.autorucFacultad de Ciencias Biológicas ; Villalobos Labra, Roberto Esteban ; 0000-0002-9638-9721 ; 250107
dc.information.autorucFacultad de Ciencias Biológicas ; Westermeier Lafuente, Francisco David ; 0000-0002-4476-4198 ; 181374
dc.information.autorucFacultad de Ciencias Biológicas ; Sáez Pedraza, Pablo José ; 0000-0003-0521-9426 ; 132607
dc.information.autorucEscuela de Medicina ; Sobrevía Luarte, Luis Alberto ; 0000-0001-5802-2243 ; 1002656
dc.information.autorucEscuela de Medicina ; Farías Jofré, Marcelo Enrique ; 0000-0003-0473-2295 ; 12286
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final148A
dc.pagina.inicio148A
dc.relation.ispartofAnnual Scientific Meeting of the Society-for-Reproductive-Investigation (°63 ; 2016 ; Montreal, Canada)
dc.revistaReproductive Sciences
dc.rightsacceso restringido
dc.titleEndothelial dysfunction and reduced insulin response in umbilical vein from the offspring of maternal obesity pregnancies
dc.typecomunicación de congreso
dc.volumen23
sipa.codpersvinculados250107
sipa.codpersvinculados181374
sipa.codpersvinculados132607
sipa.codpersvinculados1002656
sipa.codpersvinculados12286
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