Eicosapentaenoic acid is primarily responsible for hypotriglyceridemic effect of fish oil in humans
Rambjør GS, Wålen AI, Windsor SL, Harris WS
Lipids · 82 citas
Etiquetas de revisión
Financiación no declaradaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 1996-01-01 · Lipids · vol. 31 · número 1Part1 · págs. S45–9
- Editorial
- Wiley
- Citado
- 147 citas · más que el 99% de estudios similares · 10.8× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 48 trabajos
- Acceso
- De pago
- Áreas de investigación
- Fatty Acid Research and Health · Aquaculture Nutrition and Growth · Edible Oils Quality and Analysis
- Palabras clave
- eicosapentaenoic acid, docosahexaenoic acid, fish oil, triglyceride lowering, omega-3 fatty acids, olive oil, phospholipid fatty acid composition, retroconversion, VLDL cholesterol, LDL cholesterol, HDL2/HDL3 ratio, lipoproteins, dietary supplementation
- MeSH
- humans, eicosapentaenoic acid, fatty acids, triglycerides, phospholipids, fish oils, cross-over studies, single-blind method, patient compliance, adult, female, male
4 autores
- Gro S. Rambjør🇳🇴University of Oslo
- Ann I. W len🇳🇴University of Oslo
- Sheryl L. Windsor🇺🇸University of Kansas Medical Center
- William Stephen Harris🇺🇸University of Kansas Medical Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
The aim of this study was to determine whether eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), or both, were responsible for the triglyceride (TG)-lowering effects of fish oil. EPA (91% pure) and DHA (83% pure), a fish oil concentrate (FOC; 41% EPA and 23% DHA) and an olive oil (OO) placebo (all ethyl esters) were tested. A total of 49 normolipidemic subjects participated. Each subject was given placebo for 2-3 wk and one of the n-3 supplements for 3 wk in randomized, blinded trials. The target n-3 fatty acid (FA) intake was 3 g/day in all studies. Blood samples were drawn twice at the end of each supplementation phase and analyzed for lipids, lipoproteins, and phospholipid FA composition. In all groups, the phospholipid FA composition changed to reflect the n-3 FA given. On DHA supplementation, EPA levels increased to a small but significant extent, suggesting that some retroconversion may have occurred. EPA supplementation did not raise DHA levels, however. FOC and EPA produced significant decreases in both TG and very low density lipoprotein (VLDL) cholesterol (C) levels (P < 0.01) and increases in low density lipoprotein (LDL) cholesterol levels (P < 0.05). DHA supplementation did not affect cholesterol, triglyceride, VLDL, LDL, or high density lipoprotein (HDL) levels, but it did cause a significant increase in the HDL2/HDL3 cholesterol ratio. We conclude that EPA appears to be primarily responsible for TG-lowering (and LDL-C raising) effects of fish oil.
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