Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells.
Intake of trans fatty acids (TFA), which are consumed by eating foods made from partially hydrogenated vegetable oils, is associated with a higher risk of cardiovascular disease. This relation can be explained by many factors including TFA's negative effect on endothelial function and reduced n...
Guardado en:
Autores principales: | , , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Public Library of Science (PLoS)
2011
|
Materias: | |
Acceso en línea: | https://doaj.org/article/86868e0fe54b470195ad36fa839a2c6b |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:86868e0fe54b470195ad36fa839a2c6b |
---|---|
record_format |
dspace |
spelling |
oai:doaj.org-article:86868e0fe54b470195ad36fa839a2c6b2021-11-18T07:31:20ZTrans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells.1932-620310.1371/journal.pone.0029600https://doaj.org/article/86868e0fe54b470195ad36fa839a2c6b2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22216328/?tool=EBIhttps://doaj.org/toc/1932-6203Intake of trans fatty acids (TFA), which are consumed by eating foods made from partially hydrogenated vegetable oils, is associated with a higher risk of cardiovascular disease. This relation can be explained by many factors including TFA's negative effect on endothelial function and reduced nitric oxide (NO) bioavailability. In this study we investigated the effects of three different TFA (2 common isomers of C18 found in partially hydrogenated vegetable oil and a C18 isomer found from ruminant-derived-dairy products and meat) on endothelial NF-κB activation and nitric oxide (NO) production. Human endothelial cells were treated with increasing concentrations of Elaidic (trans-C18:1 (9 trans)), Linoelaidic (trans-C18:2 (9 trans, 12 trans)), and Transvaccenic (trans-C18:1 (11 trans)) for 3 h. Both Elaidic and Linoelaidic acids were associated with increasing NF-κB activation as measured by IL-6 levels and phosphorylation of IκBα, and impairment of endothelial insulin signaling and NO production, whereas Transvaccenic acid was not associated with these responses. We also measured superoxide production, which has been hypothesized to be necessary in fatty acid-dependent activation of NF-κB. Both Elaidic acid and Linoelaidic acid are associated with increased superoxide production, whereas Transvaccenic acid (which did not induce inflammatory responses) did not increase superoxide production. We observed differential activation of endothelial superoxide production, NF-κB activation, and reduction in NO production by different C18 isomers suggesting that the location and number of trans double bonds effect endothelial NF-κB activation.Naomi G IwataMatilda PhamNorma O RizzoAndrew M ChengEzekiel MaloneyFrancis KimPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 12, p e29600 (2011) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
Medicine R Science Q |
spellingShingle |
Medicine R Science Q Naomi G Iwata Matilda Pham Norma O Rizzo Andrew M Cheng Ezekiel Maloney Francis Kim Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
description |
Intake of trans fatty acids (TFA), which are consumed by eating foods made from partially hydrogenated vegetable oils, is associated with a higher risk of cardiovascular disease. This relation can be explained by many factors including TFA's negative effect on endothelial function and reduced nitric oxide (NO) bioavailability. In this study we investigated the effects of three different TFA (2 common isomers of C18 found in partially hydrogenated vegetable oil and a C18 isomer found from ruminant-derived-dairy products and meat) on endothelial NF-κB activation and nitric oxide (NO) production. Human endothelial cells were treated with increasing concentrations of Elaidic (trans-C18:1 (9 trans)), Linoelaidic (trans-C18:2 (9 trans, 12 trans)), and Transvaccenic (trans-C18:1 (11 trans)) for 3 h. Both Elaidic and Linoelaidic acids were associated with increasing NF-κB activation as measured by IL-6 levels and phosphorylation of IκBα, and impairment of endothelial insulin signaling and NO production, whereas Transvaccenic acid was not associated with these responses. We also measured superoxide production, which has been hypothesized to be necessary in fatty acid-dependent activation of NF-κB. Both Elaidic acid and Linoelaidic acid are associated with increased superoxide production, whereas Transvaccenic acid (which did not induce inflammatory responses) did not increase superoxide production. We observed differential activation of endothelial superoxide production, NF-κB activation, and reduction in NO production by different C18 isomers suggesting that the location and number of trans double bonds effect endothelial NF-κB activation. |
format |
article |
author |
Naomi G Iwata Matilda Pham Norma O Rizzo Andrew M Cheng Ezekiel Maloney Francis Kim |
author_facet |
Naomi G Iwata Matilda Pham Norma O Rizzo Andrew M Cheng Ezekiel Maloney Francis Kim |
author_sort |
Naomi G Iwata |
title |
Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
title_short |
Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
title_full |
Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
title_fullStr |
Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
title_full_unstemmed |
Trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
title_sort |
trans fatty acids induce vascular inflammation and reduce vascular nitric oxide production in endothelial cells. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2011 |
url |
https://doaj.org/article/86868e0fe54b470195ad36fa839a2c6b |
work_keys_str_mv |
AT naomigiwata transfattyacidsinducevascularinflammationandreducevascularnitricoxideproductioninendothelialcells AT matildapham transfattyacidsinducevascularinflammationandreducevascularnitricoxideproductioninendothelialcells AT normaorizzo transfattyacidsinducevascularinflammationandreducevascularnitricoxideproductioninendothelialcells AT andrewmcheng transfattyacidsinducevascularinflammationandreducevascularnitricoxideproductioninendothelialcells AT ezekielmaloney transfattyacidsinducevascularinflammationandreducevascularnitricoxideproductioninendothelialcells AT franciskim transfattyacidsinducevascularinflammationandreducevascularnitricoxideproductioninendothelialcells |
_version_ |
1718423356180529152 |