Ernährung & Medizin 2003; 18(4): 205-210
DOI: 10.1055/s-2003-45549
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Omega-3-Fettsäuren und Arteriosklerose

Omega 3 fatty acids and arteriosclerosisOlaf Adam1
  • 1Walther-Straub-Institut für Pharmakologie und Toxikologie
Further Information

Publication History

Publication Date:
04 December 2006 (online)

Zusammenfassung

Die Pathogenese der Arteriosklerose wird in einer Schädigung des Endothels mit nachfolgender Adhärenz immunkompetenter Zellen und deren Migration in subendotheliales Gewebe gesehen. Die eingewanderten Zellen setzen pro-inflammatorische Mediatoren frei, deren chemotaktische, proliferative und oxidative Signale in der Bildung arteriosklerotischer Plaques resultieren. Zu den Omega-3-Fettsäuren gehören die α-Linolen- und Eicosapentaensäure (EPA). GCP-konforme Studien der letzten Jahre haben gezeigt, dass sowohl durch erhöhte Zufuhr der a-Linolensäure als auch durch EPA eine Primär- und Sekundärprävention der Arteriosklerose erfolgreich ist. Klinische Studien weisen darauf hin, dass die Wirkung der α-Linolensäure erst nach deren Umwandlung zu EPA einsetzt. EPA wirkt den pro-inflammatorischen Signalen auf enzymatischer, transkriptioneller und genomischer Ebene entgegen. Es wird enzymatisch die Bildung pro-inflammatorischer Eicosanoide, Cytokine und Chemokine vermindert, auf transkriptioneller Ebene die Signaltransduktion herabgesetzt und auf genomischer Ebene die Proliferation der Entzündungszellen gehemmt. Daneben senken Omega-3-Fettsäuren erhöhte Triglyceridspiegel und vermindern die gesteigerte Thrombozytenaggregation. Neuere Studien zeigen, dass der Hintergrunddiät wesentliche Bedeutung zukommt. Die Menge der in der Nahrung enthaltenen Arachidonsäure bestimmt die Wirkung der zugeführten EPA. Es konnte gezeigt werden, dass eine Verminderung der Arachidonsäure in der Nahrung die Resorption der EPA aus dem Darm erhöht, deren Einbau in Zellmembranen steigert und die pro-inflammatorischen Mediatoren senkt. Der Omega-3/Omega-6-Quotient sollte entsprechend diesen Befunden weniger auf die Präkursoren als auf Arachidonsäure und EPA bezogen werden.

Summary

The pathogenesis of arteriosclerosis is defined as an impairment of the endothelium with subsequent adherence of immunologically competent cells and their migration into the subendothelial tissue. The migrated cells release proinflammatory mediators triggering chemotactic, proliferative and oxidative signals resulting in arteriosclerotic plaques. Omega fatty acids comprise the alpha-linolenic and the eicosapentaenoic acids (EPA). GCP-conforming studies performed in recent years have shown that both the increased supplementation with alpha-linolenic acid and of EPA are effective in the primary and secondary prevention of arteriosclerosis. Clinical studies have indicated that linolenic acid will only become effective when it begins to be transformed to EPA. EPA counterbalances proinflammatory signals at the enzymatic, transcriptional and genomic levels. The formation of proinflammatory eicosanoids and cytokines are enzymatically reduced, the signal transduction at the transcriptional level is diminished and, at the genomic level, the proliferation of proinflammatory cells is retarded. In addition, omega 3 fatty acids will lower high triglyceride levels, at the same time reducing an increased aggregation of thrombocytes. Recent studies indicate that background diets can play a significant role. The volume of arachidonic acid contained in the diet determines the efficacy of supplemented EPA. It could be demonstrated that a reduction of arachidonic acid in the diet increases the resorption of EPA from the bowel, promotes its incorporation in the cell membrane and lowers proinflammatory mediators. In accordance with these findings, we recommend to determine the omega 3/omega 6 quotient rather on the presence of arachidonic acid and EPA instead of that of precursors.

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Prof. Dr. Olaf Adam

Walther-Straub-Institut für Pharmakologie und Toxikologie

Nußbaumstraße 26

80336 München

Email: olaf.adam@lrz.uni-muenchen.de

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