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Details

Autor(en) / Beteiligte
Titel
Incremental replacement of saturated fats by n −3 fatty acids in high-fat, high-cholesterol diets reduces elevated plasma lipid levels and arterial lipoprotein lipase, macrophages and atherosclerosis in LDLR−/− mice
Ist Teil von
  • Atherosclerosis, 2014-06, Vol.234 (2), p.401-409
Ort / Verlag
Ireland: Elsevier Ireland Ltd
Erscheinungsjahr
2014
Link zum Volltext
Quelle
Elsevier ScienceDirect Journals Complete
Beschreibungen/Notizen
  • Abstract Objective Effects of progressive substitution of dietary n −3 fatty acids (FA) for saturated FA (SAT) on modulating risk factors for atherosclerosis have not been fully defined. Our previous reports demonstrate that SAT increased, but n −3 FA decreased, arterial lipoprotein lipase (LpL) levels and arterial LDL-cholesterol deposition early in atherogenesis. We now questioned whether incremental increases in dietary n −3 FA can counteract SAT-induced pro-atherogenic effects in atherosclerosis-prone LDL-receptor knockout (LDLR−/−) mice and have identified contributing mechanisms. Methods and results Mice were fed chow or high-fat diets enriched in SAT, n −3, or a combination of both SAT and n −3 in ratios of 3:1 (S: n −3 3:1) or 1:1 (S: n −3 1:1). Each diet resulted in the expected changes in fatty acid composition in blood and aorta for each feeding group. SAT-fed mice became hyperlipidemic. By contrast, n −3 inclusion decreased plasma lipid levels, especially cholesterol. Arterial LpL and macrophage levels were increased over 2-fold in SAT-fed mice but these were decreased with incremental replacement with n −3 FA. n −3 FA partial inclusion markedly decreased expression of pro-inflammatory markers (CD68, IL-6, and VCAM-1) in aorta. SAT diets accelerated advanced atherosclerotic lesion development, whereas all n −3 FA-containing diets markedly slowed atherosclerotic progression. Conclusion Mechanisms whereby dietary n −3 FA may improve adverse cardiovascular effects of high-SAT, high-fat diets include improving plasma lipid profiles, increasing amounts of n −3 FA in plasma and the arterial wall. Even low levels of replacement of SAT by n −3 FA effectively reduce arterial lipid deposition by decreasing aortic LpL, macrophages and pro-inflammatory markers.

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