Financiado en parte por AstraZeneca
Omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and their mechanisms of action on apolipoprotein B-containing lipoproteins in humans: a review
Oscarsson J, Hurt-Camejo E
Lipids in health and disease · 105 citas
Etiquetas de revisión
Vínculos de autores con la industriaFinanciado por la industriaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Revisión sistemática (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- AstraZeneca
- Autores
- Al menos un autor declara un vínculo económico con la industria
Según 1 financiador declarado y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2017-08-10 · Lipids Health Dis · vol. 16 · número 1 · pág. 149
- Editorial
- BioMed Central
- Citado
- 157 citas · más que el 99% de estudios similares · 8.0× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 65 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Fatty Acid Research and Health · Eicosanoids and Hypertension Pharmacology · Liver Disease Diagnosis and Treatment
- Palabras clave
- Docosahexaenoic acid, Eicosapentaenoic acid, Postprandial, Very low-density lipoprotein, Internal medicine, Endocrinology, Chemistry, Triglyceride, Hypertriglyceridemia, Lipoprotein, Chylomicron, Apolipoprotein B, Fatty acid, Cholesterol, Biochemistry, Biology, Medicine, Polyunsaturated fatty acid, Insulin
- MeSH
- liver, humans, hypertriglyceridemia, lipoprotein lipase, docosahexaenoic acids, eicosapentaenoic acid, triglycerides, chylomicrons, lipoproteins, hdl, lipoproteins, ldl, lipoproteins, vldl, apolipoproteins b, apolipoproteins e, fasting, oxidation-reduction, biotransformation, postprandial period, dietary supplements
2 autores
- Jan Oscarsson🇦🇺🇸🇪 · autor de correspondenciaAstraZeneca (Australia); AstraZeneca (Sweden)
- Eva Hurt‐Camejo🇸🇪AstraZeneca (Sweden)
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Epidemiological and genetic studies suggest that elevated triglyceride (TG)-rich lipoprotein levels in the circulation increase the risk of cardiovascular disease. Prescription formulations of omega-3 fatty acids (OM3FAs), mainly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), reduce plasma TG levels and are approved for the treatment of patients with severe hypertriglyceridemia. Many preclinical studies have investigated the TG-lowering mechanisms of action of OM3FAs, but less is known from clinical studies.
Methods
We conducted a review, using systematic methodology, of studies in humans assessing the mechanisms of action of EPA and DHA on apolipoprotein B-containing lipoproteins, including TG-rich lipoproteins and low-density lipoproteins (LDLs). A systematic search of PubMed retrieved 55 articles, of which 30 were used in the review; 35 additional arrticles were also included.
Results
In humans, dietary DHA is retroconverted to EPA, while production of DHA from EPA is not observed. Dietary DHA is preferentially esterified into TGs, while EPA is more evenly esterified into TGs, cholesterol esters and phospholipids. The preferential esterification of DHA into TGs likely explains the higher turnover of DHA than EPA in plasma. The main effects of both EPA and DHA are decreased fasting and postprandial serum TG levels, through reduction of hepatic very-low-density lipoprotein (VLDL)-TG production. The exact mechanism for reduced VLDL production is not clear but does not include retention of lipids in the liver; rather, increased hepatic fatty acid oxidation is likely. The postprandial reduction in TG levels is caused by increased lipoprotein lipase activity and reduced serum VLDL-TG concentrations, resulting in enhanced chylomicron clearance. Overall, no clear differences between the effects of EPA and DHA on TG levels, or on turnover of TG-rich lipoproteins, have been observed. Effects on LDL are complex and may be influenced by genetics, such as APOE genotype.
Conclusions
EPA and DHA diminish fasting circulating TG levels via reduced production of VLDL. The mechanism of reduced VLDL production does not involve hepatic retention of lipids. Lowered postprandial TG levels are also explained by increased chylomicron clearance. Little is known about the specific cellular and biochemical mechanisms underlying the TG-lowering effects of EPA and DHA in humans.
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