Author
VEMURI, MADHURI - UCD, NUTR. DEPT. | |
Kelley, Darshan |
Submitted to: Book Chapter
Publication Type: Book / Chapter Publication Acceptance Date: 2/1/2007 Publication Date: 11/19/2007 Citation: Vemuri, M., Kelley, D.S. 2007. The Effects of Dietary Fatty Acids on Lipid Metabolism. Book Chapter in, "Fatty Acids in Foods and their Health Implications, third edition". CRC Press Taylor & Francis Group pp.591-630. Interpretive Summary: Dietary fats have profound effects on lipid metabolism. The inhibition of endogenous fatty acid synthesis by exogenous dietary fat is now well understood. However, there is some controversy about whether dietary saturated fat is effective in suppressing de novo fatty acid synthesis, but the suppression of liver fatty acid synthesis by dietary PUFAs, particularly linoleic acid is well established. Depending on their degree of unsaturation and chain length, dietary fatty acids can affect blood lipids and lipoprotein levels. Both saturated fatty acids (12:0-16:0) and dietary cholesterol increase blood cholesterol and polyunsaturated fatty acids reduce it. Trans fatty acids, even though are polyunsaturated, increase LDL and decrease HDL cholesterol, possibly because of the presence of trans bonds affecting metabolism. Monounsaturated fatty acids, mainly oleic acid (18:1n-9) reduce total- and increase HDL cholesterol. Most studies with long chain n-3 PUFA did not find a change in total cholesterol, but both the LDL and HDL cholesterols were increased and triglycerides were reduced in those studies. Studies with purified DHA and EPA supplementation found both fatty acids were effective in reducing plasma triglycerides, although some found DHA to be more effective than EPA. These studies also indicated that it is only DHA that reduced the number of small dense LDL particles and increased the concentration of HDL-2, increased blood flow and reduced heart rate. Technical Abstract: Depending on their degree of unsaturation and chain length, dietary fatty acids can affect blood lipids and lipoprotein levels. Both saturated fatty acids (12:0-16:0) and dietary cholesterol increase blood cholesterol and polyunsaturated fatty acids reduce it. Trans fatty acids, even though are polyunsaturated, increase LDL and decrease HDL cholesterol, possibly because of the presence of trans bonds affecting metabolism. Monounsaturated fatty acids, mainly oleic acid (18:1n-9) reduce total- and increase HDL cholesterol. Most studies with long chain n-3 PUFA did not find a change in total cholesterol, but both the LDL and HDL cholesterols were increased and triglycerides were reduced in those studies. Studies with purified DHA and EPA supplementation found both fatty acids were effective in reducing plasma triglycerides, although some found DHA to be more effective than EPA. These studies also indicated that it is only DHA that reduced the number of small dense LDL particles and increased the concentration of HDL-2, increased blood flow and reduced heart rate. Increased consumption of n-6 PUFAs has been found to enhance the production of inflammatory eicosanoids like PGE2, and LTB4, while EPA and DHA reduced the tissue concentration of AA and production of inflammatory eicosanoids. N-3 PUFAs have also been found to reduce the expression of genes for inflammatory cytokines (IL-1', IL-6, TNF-') and have anti-thrombotic and anti-arrhythmic effects. Despite the high degree of unsaturation and susceptibility to oxidation, EPA and DHA have been reported by some investigators to reduce oxidative stress. Evidence from a number of epidemiological, prospective and intervention studies clearly show that increased intake of long chain n-3 PUFAs reduces the risk for CVD. Because of limited elongation of ALA to EPA and DHA, its health effects are not as dramatic as those of the long chain n-3 PUFA. Despite the knowledge of the many health benefits of n-3 PUFAs, their consumption remains at a minimal level in the United States. On the other hand, consumption of pro-inflammatory n-6 PUFAs has markedly increased. The reduced intake of n-3 PUFAs and increased intake of n-6 PUFA over the last several decades may be the major reason for the increase in inflammatory diseases. Thus, an increase in the consumption of n-3 PUFAs and a decrease in the consumption of n-6 PUFAs are needed to balance the ratio between the consumption of these two groups of fatty acids. Reduction in the consumption of trans fatty acids and saturated fatty acid will also reduce the risk for CVD. Further studies are needed to determine the dose dependent effects of n-3 PUFAs, interaction between n-3 and n-6 PUFAs, and the underlying mechanisms. |