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Eighteen-carbon trans fatty acids and inflammation in the context of atherosclerosis

Eighteen-carbon trans fatty acids and inflammation in the context of atherosclerosis
Eighteen-carbon trans fatty acids and inflammation in the context of atherosclerosis
Endothelial dysfunction is a proinflammatory state characterized by chronic activation of the endothelium, which leads to atherosclerosis and cardiovascular disease (CVD). Intake of trans fatty acids (TFAs) is associated with an increased risk of CVD. This risk is usually associated with industrial TFAs (iTFAs) rather than ruminant TFAs (rTFAs); however it is not clear how specific TFA isomers differ in their biological activity and mechanisms of action with regard to inflammation. Here we review the literature on 18carbon TFAs, including the research associating their intake or levels with CVD and studies relating 18carbon TFA exposure to modulation of inflammatory processes. The evidence associating iTFAs with CVD risk factors is fairly consistent and studies in humans usually show a relation between iTFAs and higher levels of inflammatory markers. In contrast, studies in humans, animals and in vitro suggest that rTFAs have null or mildly beneficial effects in cardiovascular health, metabolic parameters and inflammatory markers, although the evidence is not always consistent. More studies are needed to better identify the beneficial and detrimental effects of the different TFAs, including those with 18 carbons.
0163-7827
Valenzuela, Carina, Alejandra
1a12a9b9-6504-4392-90c5-246644b0ad5c
Baker, Ella
7cd5b762-d7d7-4584-b9a7-dba555085440
Miles, Elizabeth
20332899-ecdb-4214-95bc-922dde36d416
Calder, Philip
1797e54f-378e-4dcb-80a4-3e30018f07a6
Valenzuela, Carina, Alejandra
1a12a9b9-6504-4392-90c5-246644b0ad5c
Baker, Ella
7cd5b762-d7d7-4584-b9a7-dba555085440
Miles, Elizabeth
20332899-ecdb-4214-95bc-922dde36d416
Calder, Philip
1797e54f-378e-4dcb-80a4-3e30018f07a6

Valenzuela, Carina, Alejandra, Baker, Ella, Miles, Elizabeth and Calder, Philip (2019) Eighteen-carbon trans fatty acids and inflammation in the context of atherosclerosis. Progress in Lipid Research, 76, [101009]. (doi:10.1016/j.plipres.2019.101009).

Record type: Review

Abstract

Endothelial dysfunction is a proinflammatory state characterized by chronic activation of the endothelium, which leads to atherosclerosis and cardiovascular disease (CVD). Intake of trans fatty acids (TFAs) is associated with an increased risk of CVD. This risk is usually associated with industrial TFAs (iTFAs) rather than ruminant TFAs (rTFAs); however it is not clear how specific TFA isomers differ in their biological activity and mechanisms of action with regard to inflammation. Here we review the literature on 18carbon TFAs, including the research associating their intake or levels with CVD and studies relating 18carbon TFA exposure to modulation of inflammatory processes. The evidence associating iTFAs with CVD risk factors is fairly consistent and studies in humans usually show a relation between iTFAs and higher levels of inflammatory markers. In contrast, studies in humans, animals and in vitro suggest that rTFAs have null or mildly beneficial effects in cardiovascular health, metabolic parameters and inflammatory markers, although the evidence is not always consistent. More studies are needed to better identify the beneficial and detrimental effects of the different TFAs, including those with 18 carbons.

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More information

Accepted/In Press date: 19 September 2019
e-pub ahead of print date: 2 November 2019

Identifiers

Local EPrints ID: 434544
URI: http://eprints.soton.ac.uk/id/eprint/434544
ISSN: 0163-7827
PURE UUID: b62eeca4-405b-45dd-9b4d-6d2c2077776b
ORCID for Ella Baker: ORCID iD orcid.org/0000-0003-1008-5506
ORCID for Elizabeth Miles: ORCID iD orcid.org/0000-0002-8643-0655
ORCID for Philip Calder: ORCID iD orcid.org/0000-0002-6038-710X

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Date deposited: 01 Oct 2019 16:30
Last modified: 17 Mar 2024 02:42

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Contributors

Author: Carina, Alejandra Valenzuela
Author: Ella Baker ORCID iD
Author: Elizabeth Miles ORCID iD
Author: Philip Calder ORCID iD

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