Key points are not available for this paper at this time.
We sought to test the hypothesis that dietary long-chain n-3 PUFA (LC n-3 PUFA) in fish oil stimulate the gene expression of lipoprotein lipase (LPL) in human adipose tissue (AT). In a randomized, double blind, placebo-controlled, cross-over study, 51 male subjects expressing an atherogenic lipoprotein phenotype (ALP) had their diets supplemented with fish oil for 6 weeks. As we previously reported for this group, supplementation with LC n-3 PUFA produced a decrease in fasting plasma triglyceride (TG) (−35%, P < 0.05), attenuation of the postprandial TG response (area and incremental area under the curve; AUC and IAUC, P < 0.05), and a decrease in small, dense LDL. The present study extended these observations by showing that these changes were accompanied by a marked increase in the concentration of LPL mRNA in adipose tissue (AT-LPL mRNA, +55%, P = 0.003) and post-heparin LPL activity (PH-LPL, +31%, P = 0.036). There was also evidence of an association between LPL gene expression and polymorphism in the apolipoprotein E gene.We conclude that the favorable influence of dietary n-3 PUFA on the ALP may be mediated, in part, through an increase in the plasma activity and gene expression of lipoprotein lipase in human adipose tissue. We sought to test the hypothesis that dietary long-chain n-3 PUFA (LC n-3 PUFA) in fish oil stimulate the gene expression of lipoprotein lipase (LPL) in human adipose tissue (AT). In a randomized, double blind, placebo-controlled, cross-over study, 51 male subjects expressing an atherogenic lipoprotein phenotype (ALP) had their diets supplemented with fish oil for 6 weeks. As we previously reported for this group, supplementation with LC n-3 PUFA produced a decrease in fasting plasma triglyceride (TG) (−35%, P < 0.05), attenuation of the postprandial TG response (area and incremental area under the curve; AUC and IAUC, P < 0.05), and a decrease in small, dense LDL. The present study extended these observations by showing that these changes were accompanied by a marked increase in the concentration of LPL mRNA in adipose tissue (AT-LPL mRNA, +55%, P = 0.003) and post-heparin LPL activity (PH-LPL, +31%, P = 0.036). There was also evidence of an association between LPL gene expression and polymorphism in the apolipoprotein E gene. We conclude that the favorable influence of dietary n-3 PUFA on the ALP may be mediated, in part, through an increase in the plasma activity and gene expression of lipoprotein lipase in human adipose tissue. First described by Austin et al. (1Austin M.A. King M.C. Vranizan K.M. Krauss R.M. Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease..Circulation. 1990; 82: 495-506Crossref PubMed Scopus (1168) Google Scholar), the atherogenic lipoprotein phenotype (ALP) defines a collection of abnormalities in plasma lipoproteins that confers a 3- to 6-fold increase in risk of coronary heart disease (CHD) and features moderately raised plasma triglyceride (TG), low HDL cholesterol (HDL-C), and predominance of small, dense LDL (2Griffin B.A. Freeman D.J. Tait G.W. Thomson J. Packard C.J. Shepherd J. Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions: relative contribution of small, dense LDL to coronary heart disease risk..Atherosclerosis. 1994; 106: 241-253Abstract Full Text PDF PubMed Scopus (497) Google Scholar, 3Austin M.A. Breslow J.L. Hennekens C.H. Buring J.E. Willet W.C. Krauss R.M. Low density lipoprotein subclass patterns and risk of myocardial infarction..J. Am. Med. Ass. 1988; 260: 1917-1921Crossref PubMed Scopus (1548) Google Scholar). An ALP originates from defects in TG metabolism that include the impaired clearance of TG-rich lipoproteins in the postprandial period, coupled with an oversupply of lipid substrates for the production of TG and thus secretion of apolipoprotien B (apoB) as TG-rich VLDL in the liver (4Packard C.J. Shepherd J. Lipoprotein heterogeneity and apolipoprotein B metabolism..Arterioscler. Thromb. Vasc. Biol. 1997; 17: 3542-3556Crossref PubMed Scopus (332) Google Scholar). Although the underlying molecular basis for these defects is not yet understood, interplay between insulin resistance and nutrient-gene interactions is likely to be central to the development and, potentially, to the correction of this high-risk dyslipidemia. Variation in response to different dietary fats is being increasingly ascribed to genetic heterogeneity and nutrient-gene interactions (5Jump D.B. Clarke S.D. Regulation of gene expression by dietary fatty acids..Ann. Rev. Nutr. 1999; 19: 64-83Crossref Scopus (546) Google Scholar). While direct evidence for the role of dietary fatty acids and their derivatives as regulators of gene expression in humans is still lacking, it is likely that many of the potentially beneficial effects of long-chain n-3 PUFA (LC n-3 PUFA) on TG metabolism are mediated through the control of gene transcription and post-transcriptional events. Fish oil supplements have been shown to correct many of the metabolic sequelae associated with insulin resistance (6Collier G.R. Sinclair A.J. Role of N-6 and N-3 fatty acids in the dietary treatment of metabolic disorders..Ann. NY Acad. Sci. 1993; 683: 322-330Crossref PubMed Scopus (12) Google Scholar), which includes decreasing the concentration of plasma TG in the pre and postprandial periods (7Harris W.S. Connor W.E. Alam N. Illingworth D.R. Reduction of postprandial triglyceridemia in humans by dietary n-3 fatty acids..J. Lipid Res. 1988; 29: 1451-1460Abstract Full Text PDF PubMed Google Scholar). Fish oil may induce a reduction in VLDL by suppressing lipogenesis and by enhancing the oxidation of fatty acids, both of which are controlled at the level of gene transcription in the liver (8Clarke S.D. Jump T.D. Polyunsaturated fatty acids regulate lipogenic and peroxisomal gene expression by independent mechansisms..Prostaglandins Leukot. Essent. Fatty Acids. 1997; 57: 65-69Abstract Full Text PDF PubMed Scopus (57) Google Scholar). While these events will indirectly increase the capacity to clear plasma TG in the postprandial period, as a result of reduced competition for lipoprotein lipase (LPL), LC n-3 PUFA may also exert direct effects on the removal of TG-rich lipoproteins through stimulation of LPL in peripheral tissues (9Harris W.S. Lu G. Rambjor G.S. Walen A.I. Ontko J.A. Chang Q. Windsor S.L. Influence of n-3 fatty acid supplementation on the endogenous activities of plasma lipases..Am. J. Clin. Nutr. 1997; 66: 254-260Crossref PubMed Scopus (112) Google Scholar). LPL activity is a rate-limiting determinant of the hydrolysis of TG in the plasma compartment. Although in quantitative terms the mass of muscle LPL far outweighs that of LPL in adipose tissue (AT-LPL), the latter removes relatively more TG in the postprandial period than skeletal muscle (10.Frayn, K. N. 1996. Integration of carbohydrate, fat and protein metabolism in the whole body. In Metabolic Regulation: A Human Perspective. K. Snell, editor. Portland Press, UK. 103–140. Google Scholar), making AT-LPL a prime target for metabolic regulation. While this is well known to occur acutely in response to insulin, considerably less is known about longer term regulation mediated by the effects of dietary fatty acids on the AT-LPL gene. There is evidence from animal studies (11Raclot T. Groscolas R. Langin D. Ferre P. Site-specific regulation of gene expression by n-3 polyunsaturated fatty acids in rat white adipose tissues..J. Lipid Res. 1997; 38: 1963-1972Abstract Full Text PDF PubMed Google Scholar, 12Murphy M.C. Zampelas A. Puddicombe S.M. Furlonger N.P. Morgan L.M. Williams C.M. Pre-translational regulation of the expression of the lipoprotein lipase (EC 3.1.1.34) gene by dietary fatty acids in the rat..Br. J. Nutr. 1993; 70: 727-736Crossref PubMed Scopus (38) Google Scholar) and, more recently, from preliminary findings in small groups of normal (13Murphy M.C. Brooks C.N. Rockett J.C. Chapman C. Lovegrove J.A. Gould B.J. Wright J.W. Williams C.M. The quantitation of lipoprotein lipase mRNA in biopsies of human adipose tissue, using the polymerase chain reaction, and the effect of increased consumption of n-3 polyunsaturated fatty acids..Eur. J. Clin. Invest. 1999; 53: 441-447Google Scholar) and diabetic humans (14Luo J. Salwa W.R. Vidal H. Oppert J-M. Colas C. Guerre-Millo M. Chapuis A-S. Chevalier A. Durand G. Slama G. Moderate intake of n-3 fatty acids for 2 months has no detrimental effect on glucose metabolism and could ameliorate the lipid profile of type 2 diabetic men..Diabetes Care. 1998; 21: 717-724Crossref PubMed Scopus (103) Google Scholar) to suggest that dietary LC n-3 PUFAs increase post-heparin LPL (PH-LPL) activity and the expression of the AT-LPL gene in the longer term, though other studies have shown no effect on PH-LPL activity (15Weintraub M.S. Zechner R. Brown A. Eisenberg S. Breslow J.L. Dietary polyunsaturated fats of the omega-6 and omega-3 series reduce postprandial lipoprotein levels. Chronic and acute effects of fat saturation on postprandial lipoprotein metabolism..J. Clin. Invest. 1988; 82: 1884-1893Crossref PubMed Scopus (290) Google Scholar, 16Nozaki S. Garg A. Vega G.L. Grundy S.M. Postheparin lipoltyic activity and plasma lipoprotein response to w-3 polyunsaturated fatty acids in patients with primary hypertriglyceridemia..Am. J. Clin. Nutr. 1991; 53: 638-642Crossref PubMed Scopus (58) Google Scholar). The purpose of this study was to extend our previous observations on the effects of fish oil supplementation on the ALP (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar) with the aim of determining whether these effects could be explained by an increase in AT-LPL gene expression. In view of our previous report of an influence of apoE polymorphism on the metabolic response to fish oil in this group (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar), the data herein includes examination of AT-LPL gene expression in relation to apoE genotype. Normal, male subjects expressing the ALP = moderately raised plasma TG low and predominance of small, dense were as previously described (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). The study was by the of and and to The study was a randomized, double blind, with periods by a the subjects supplemented their with 6 of fish oil in the of of a acid acid TG long-chain n-3 PUFA) 6 of oil as a the period, subjects were to the were from subjects at and 6 of In a postprandial PH-LPL activity and adipose tissue biopsies for LPL gene expression were at the of The for the postprandial and of plasma LDL and PH-LPL activity have been described in previously (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). adipose tissue biopsies were under from the of the between and at the on of the The of this tissue was on the that it and to the of white adipose tissue was from a 2 The was by a adipose tissue was and in and at was from of tissue using a of the of and P. N. of by acid PubMed Scopus Google Scholar). tissue were in a with and in were in and in were at using the mRNA for LPL was by transcription by polymerase chain was using the by et al. M. D. Vega N. Vidal H. regulation of and lipoprotein lipase mRNA in human Clin. Invest. PubMed Scopus Google Scholar), by The production of this from the has been previously described by Murphy et al. (13Murphy M.C. Brooks C.N. Rockett J.C. Chapman C. Lovegrove J.A. Gould B.J. Wright J.W. Williams C.M. The quantitation of lipoprotein lipase mRNA in biopsies of human adipose tissue, using the polymerase chain reaction, and the effect of increased consumption of n-3 polyunsaturated fatty acids..Eur. J. Clin. Invest. 1999; 53: 441-447Google Scholar). that both the and the target in the reaction, of different and transcription and were using the First was at for and at for 2 The were in the of polymerase in the of at for and at for 2 were to in an In mRNA was in as an using and under The were on with and with a were from the using The of the density of the to the was the of the The LPL mRNA were and relative to the concentration of mRNA of was an was from by the A for from human Res. Scopus Google Scholar). ApoE was by and by as previously described A for the of of apoE from to and by Scopus Google Scholar). The for plasma and LPL gene expression are on 51 subjects tissue biopsies both on post-heparin LPL (PH-LPL) activity was on a of are as of data was by normal and data was for LPL between data oil were by for between apoE were by between were by and and The for the subjects have been described in our previous report (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). In with the study subjects moderately raised plasma TG low and a predominance of small, dense LDL LDL subclass Although subjects could be as being at < subjects were and on ALP group a of the polymorphism of the as with the and to no at the of period not The fish oil and control supplements were well and as by and fatty acid was There was no evidence of effects The lipid and lipoprotein response to fish oil in this group has been reported (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). data shown with the of the PH-LPL to a of 51 Fish oil supplementation produced a decrease in fasting plasma TG P < and a marked decrease in the concentration of postprandial plasma TG triglyceride area and incremental = = = TG = oil oil = oil oil oil = LPL = LPL = mRNA mRNA = oil triglyceride (TG) area and incremental area under the postprandial TG and lipoprotein lipase activity and and adipose tissue lipoprotein lipase mRNA in group and and of the are P P P oil in a triglyceride (TG) area and incremental area under the postprandial TG and lipoprotein lipase activity and and adipose tissue lipoprotein lipase mRNA in group and and of the are in fatty acid have been reported previously (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). fish oil supplementation increased the concentration of LC n-3 PUFA and acids in relative to the LC n-3 PUFA increased by < the of to LC n-3 PUFA in by to plasma was from a of subjects for the of LPL activity at the of the fish oil and control PH-LPL activity at an increase P < in response to fish oil supplementation relative to the control PH-LPL activities were than at the between treatment groups was no longer The group an increase P = 0.003) in the concentration of AT-LPL mRNA fish oil relative to the control the of the control period, the concentration of AT-LPL mRNA was = P = 0.003) with the of postprandial There was a = P = between the changes oil and in PH-LPL activity and concentration of AT-LPL mRNA There was no between PH-LPL activity and fasting of the of postprandial As shown previously (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar), the of for the apoE polymorphism in this group of ALP subjects was for a with of the group being for the genotype. There were no for the were for the with the being for the There was evidence that of the a different lipoprotein response to fish oil than (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). this subjects were as = = The effect of apoE on the lipid response to fish oil in this group has been reported previously (17Minihane A.M. Khan S. Leigh-Firbank C. Talmud P. Wright J.W. Murphy M.C. Griffin B.A. Williams C.M. ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype..Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1990-1997Crossref PubMed Scopus (197) Google Scholar). In the present study, being no in plasma TG and the of postprandial between and the LPL response to fish oil was in the to of the a increase in PH-LPL activity at of = and While the level of AT-LPL mRNA increased in apoE on fish the response with a increase in gene expression and P < were between LPL mRNA and the of postprandial in the control = P < 0.05), and in the fish oil = P < LPL mRNA was with PH-LPL activity in fish oil = P < The of an ALP in may that of insulin resistance A. of of insulin resistance to coronary heart disease 1994; PubMed Scopus Google Scholar). Although this may have a it is likely to the of risk and Fish oil ameliorate the lipid abnormalities associated with this by suppressing the of TG in the liver and the of postprandial (7Harris W.S. Connor W.E. Alam N. Illingworth D.R. Reduction of postprandial triglyceridemia in humans by dietary n-3 fatty acids..J. Lipid Res. 1988; 29: 1451-1460Abstract Full Text PDF PubMed Google Scholar). The present study sought to evidence for the latter and to the molecular basis of this effect with on the LPL adipose tissue an of postprandial this was as a and tissue for this PH-LPL activity has been as a of postprandial in insulin P. J. S. J. of with insulin resistance PubMed Scopus Google Scholar, T. S. N. K. S. S. M. M. T. K. K. plasma protein in Thromb. Vasc. Biol. 1994; Google Scholar, Brown and lipoprotein Thromb. Vasc. Biol. Google Scholar). PH-LPL have also been reported in a of with coronary and have been to changes in plasma and lipoproteins J.W. H. Lipoprotein lipase activity is in a of patients with coronary disease and is associated with changes in and Lipid Res. 1999; Full Text Full Text PDF PubMed Google Scholar). the of this it to that of the LPL be beneficial by this studies on the effects of fish oil on PH-LPL activity in patients and groups have to the of the post-heparin While for PH-LPL activity in the present study were of a to reported a direct with to the relative of in these ALP subjects was not to in LPL and the subjects under There was a increase in PH-LPL activity in response to the fish which was than that reported in the The of studies report no effect of fish oil on and conclude that the from a influence in suppressing TG W.S. Fish and plasma lipid and lipoprotein metabolism in a Lipid Res. Full Text PDF PubMed Google Scholar, J.A. Dietary fish events in the of low density lipoproteins and target B for the of Lipid Res. 1999; Full Text Full Text PDF PubMed Google Scholar). in LPL activity in response to fish oil have been in pre and post-heparin plasma (9Harris W.S. Lu G. Rambjor G.S. Walen A.I. Ontko J.A. Chang Q. Windsor S.L. Influence of n-3 fatty acid supplementation on the endogenous activities of plasma lipases..Am. J. Clin. Nutr. 1997; 66: 254-260Crossref PubMed Scopus (112) Google Scholar, A. Morgan L.M. Murphy M.C. Williams C.M. of dietary fatty acid on postprandial insulin, and lipoprotein lipase J. Clin. Nutr. 1994; Scholar), though the between these is In view of the role of LPL as a rate-limiting determinant of TG removal in the plasma it was to an between PH-LPL activity and plasma though the present data evidence to a LPL activity in plasma at and is to a and of LPL from the of skeletal muscle and adipose tissue, the relative activities of which will with previous and the of the may metabolic between PH-LPL and plasma are not more the tissue skeletal muscle has considerably more as the of LPL and of plasma TG and lipoprotein in response to and P. H. Lipoprotein lipase activity and triglyceride fat and diets in PubMed Scopus Google Scholar, human lipoprotein lipase gene expression in skeletal muscle not adipose J. Google Scholar, M. H. J. A between the effects of and on insulin in patients with and Full Text PDF PubMed Scopus Google Scholar, C.M. T. S. J. Packard C.J. Shepherd J. and coronary 1990; Full Text PDF PubMed Scopus Google Scholar). with the of reported has on lipid metabolism in the and no of postprandial events in adipose tissue that may be of to the of dietary fatty acids on the of TG in the postprandial Although LPL activity to adipose tissue was not in the present study, it is to that this be more associated with changes in postprandial and AT-LPL gene expression. While dietary LC n-3 PUFA are the to pre and events (5Jump D.B. Clarke S.D. Regulation of gene expression by dietary fatty acids..Ann. Rev. Nutr. 1999; 19: 64-83Crossref Scopus (546) Google Scholar), evidence for their effects on LPL gene expression in in human tissues is study to findings from our that effects of fish oil on the regulation of LPL gene expression in the of M.C. Zampelas A. Puddicombe S.M. Furlonger N.P. Morgan L.M. Williams C.M. Pre-translational regulation of the expression of the lipoprotein lipase (EC 3.1.1.34) gene by dietary fatty acids in the rat..Br. J. Nutr. 1993; 70: 727-736Crossref PubMed Scopus (38) Google Scholar). In a study on a small group of male subjects = the level of AT-LPL mRNA was shown to increase in of subjects in response to fish oil (13Murphy M.C. Brooks C.N. Rockett J.C. Chapman C. Lovegrove J.A. Gould B.J. Wright J.W. Williams C.M. The quantitation of lipoprotein lipase mRNA in biopsies of human adipose tissue, using the polymerase chain reaction, and the effect of increased consumption of n-3 polyunsaturated fatty acids..Eur. J. Clin. Invest. 1999; 53: 441-447Google Scholar). changes in the level of AT-LPL mRNA were associated with changes in fasting plasma TG and postprandial that LPL gene expression may control changes in the of and endogenous In the present study, the level of LPL mRNA increased by on fish oil relative to the oil There are no other studies with a with to these In a study, et al. (14Luo J. Salwa W.R. Vidal H. Oppert J-M. Colas C. Guerre-Millo M. Chapuis A-S. Chevalier A. Durand G. Slama G. Moderate intake of n-3 fatty acids for 2 months has no detrimental effect on glucose metabolism and could ameliorate the lipid profile of type 2 diabetic men..Diabetes Care. 1998; 21: 717-724Crossref PubMed Scopus (103) Google Scholar) reported an increase in the level of LPL mRNA in adipose tissue in a small group of type = 2 months of supplementation with fish oil relative to oil fish to LC n-3 evidence for the effects of LC n-3 PUFA on AT-LPL mRNA from studies and animal the of which are the effects are to adipose tissue R. The expression of lipoprotein for and lipoprotein 1997; PubMed Scopus Google Scholar). on that dietary fatty acids influence their effects on of LPL to be a more of regulation in adipose tissue S. Lipoprotein lipase gene regulators at the and post-transcriptional 1993; PubMed Scopus Google Scholar, C. G. Fatty acids regulate the expression of lipoprotein lipase gene and activity in and adipose J. PubMed Scopus Google Scholar, H. T. different are in regulation of lipoprotein lipase in adipose J. PubMed Scopus Google Scholar). In with our the level of AT-LPL mRNA from humans was to the incremental area under the postprandial the control period In the in gene expression oil was to the in PH-LPL activity Although these could be as under to of LPL is not in Regulation of the and of lipoprotein J. PubMed Scopus Google Scholar), that dietary LC n-3 PUFA LPL activity and plasma TG in the longer term through regulation of events. In the present study, the response of both PH-LPL and AT-LPL mRNA to was to apoE genotype. The relatively PH-LPL activity and of AT-LPL than and the by which LC n-3 PUFA in fish oil may exert effects in this group are and of In this study evidence to suggest that dietary LC n-3 PUFAs in increase AT-LPL gene expression and PH-LPL effects may be by the apoE polymorphism and could to the correction of lipid abnormalities associated with the The the and for this and to for the oil is by the atherogenic lipoprotein phenotype adipose tissue area under acid acid incremental area under the long-chain post-heparin lipoprotein lipase
Khan et al. (Sat,) studied this question.