Adipose Tissue and Fatty Acids in Cardiovascular Disease
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AbstractCardiovascular disease is the main cause of death globally and addressing risk factors can prevent disease. Obesity is a major risk factor and a growing health problem in both developed and developing countries and adipose tissue produces a variety of biologically active substances relevant in cardiovascular disease. The main aim of the thesis was to shed light on the biological role of fatty acids in myocardial infarction and remodeling, taking a prime interest in the interactions between the immune system and adipose tissue. Specifically, the aim was to study the effects of omega-3 fatty acids after myocardial infarction during myocardial remodeling in an experimental rat infarction model. Furthermore, we investigated if the levels of fatty acids and cardiovascular mediators are modulated in adipose tissue in patients with heart failure by retrieving tissue samples from adipose tissue in proximity to the heart and to the skin. And last, our aim was to provide “proof-of-concept” that fatty acid-derived pro-resolving lipid mediators are biosynthesized during acute myocardial infarction in humans by sampling blood. The thesis demonstrate that supplementation with omega-3 fatty acids leads to a proportional increase of omega-3 fatty acids in myocardial tissue and attenuates left ventricle remodeling after myocardial infarction. Second, adipose tissue from the heart and skin displays molecular similarities in patients with heart failure and controls. However, depot-specific differences of possible importance were demonstrated. And third, omega-3 fatty acid derived pro-resolving lipid mediators play a role in acute myocardial infarction and their temporal dynamics in blood provide a potential target for modulation and therapeutic interventions. Overall, our results suggest a potential role for fatty acids and fatty acid-derived mediators after myocardial infarction and during myocardial remodeling.
List of papers
|Paper I: Krill oil attenuates left ventricular dilatation after myocardial infarction in rats. Fosshaug LE, Berge RK, Beitnes JO, Berge K, Vik H, Aukrust P, Gullestad L, Vinge LE, Øie E. Lipids Health Dis. 2011;10:245. DOI: 10.1186/1476-511X-10-245. The article is included in the thesis. Also available at https://doi.org/10.1186/1476-511X-10-245|
|Paper II: Altered levels of fatty acids and inflammatory and metabolic mediators in epicardial adipose tissue in patients with systolic heart failure. Fosshaug LE, Dahl CP, Risnes I, Bohov P, Berge RK, Nymo S, Geiran O, Yndestad A, Gullestad L, Aukrust P, Vinge LE, Øie E. J Card Fail. 2015;21:916-23. DOI: 10.1016/j.cardfail.2015.07.014. The article is not available in DUO due to publisher restrictions. The published version is available at: https://doi.org/10.1016/j.cardfail.2015.07.014|
|Paper III: Early increase of specialized pro-resolving lipid mediators in patients with ST-elevation myocardial infarction. Fosshaug LE, Colas RA, Anstensrud AK, Gregersen I, Nymo S, Sagen EL, Michelsen A, Vinge LE, Øie E, Gullestad L, Halvorsen B, Hansen TV, Aukrust P, Dalli J, Yndestad A. EBioMedicine. 2019 Aug; 46: 264–273. DOI: 10.1016/j.ebiom.2019.07.024. The unpublished paper is included in the thesis. The article is available at: https://doi.org/10.1016/j.ebiom.2019.07.024|