Effect of apoC-III gene polymorphisms on the lipoprotein-lipid profile of viscerally obese men

Abdominal visceral adipose tissue (AT) accumulation is associated with an atherogenic metabolic profile that includes increased plasma triglyceride (TG), low HDL cholesterol levels, and an insulin-resistant hyperinsulinemic state. Whereas the apolipoprotein (apo) C-III C3238G gene variant, often referred to as the SstI polymorphism, has been related to variations in plasma TG concentrations, another variation within the insulin responsive element (C-482T) of the apoC-III gene has been associated with greater glucose and insulin responses to an oral glucose tolerance test (OGTT); however, these results were obtained in nonobese individuals. We therefore investigated the effects of three apoC-III gene polymorphisms, namely SstI, C-482T, and T-455C, on fasting plasma lipoprotein-lipid levels and response to a 75 g OGTT in a sample of 122 viscerally obese men (abdominal visceral AT area ≥130 cm2). Among the three gene variants that were examined, the SstI variation was the only one found to be associated with hypertriglyceridemia. Indeed, S1/S2 heterozygotes (n = 24) were characterized by increased fasting plasma TG concentrations compared with S1/S1 homozygotes (n = 98) (mean ± SD: 3.03 ± 1.58 vs. 2.34 ± 0.95 mmol/l respectively, P < 0.05). The higher TG concentrations in S1/S2 were associated with the presence of smaller, denser LDL particles compared with S1/S1 subjects (LDL peak particle diameter: 24.8 ± 0.5 nm vs. 25.1 ± 0.5 nm respectively, P < 0.05). Furthermore, there was no association between the response to the OGTT and any of the apoC-III gene variants (SstI, T-455C, or C-482T) examined.Results of the present study support the notion of a hypertriglyceridemic effect associated with the apoC-III SstI polymorphism that could modulate the magnitude of the dyslipidemic state in abdominally obese patients. Abdominal visceral adipose tissue (AT) accumulation is associated with an atherogenic metabolic profile that includes increased plasma triglyceride (TG), low HDL cholesterol levels, and an insulin-resistant hyperinsulinemic state. Whereas the apolipoprotein (apo) C-III C3238G gene variant, often referred to as the SstI polymorphism, has been related to variations in plasma TG concentrations, another variation within the insulin responsive element (C-482T) of the apoC-III gene has been associated with greater glucose and insulin responses to an oral glucose tolerance test (OGTT); however, these results were obtained in nonobese individuals. We therefore investigated the effects of three apoC-III gene polymorphisms, namely SstI, C-482T, and T-455C, on fasting plasma lipoprotein-lipid levels and response to a 75 g OGTT in a sample of 122 viscerally obese men (abdominal visceral AT area ≥130 cm2). Among the three gene variants that were examined, the SstI variation was the only one found to be associated with hypertriglyceridemia. Indeed, S1/S2 heterozygotes (n = 24) were characterized by increased fasting plasma TG concentrations compared with S1/S1 homozygotes (n = 98) (mean ± SD: 3.03 ± 1.58 vs. 2.34 ± 0.95 mmol/l respectively, P < 0.05). The higher TG concentrations in S1/S2 were associated with the presence of smaller, denser LDL particles compared with S1/S1 subjects (LDL peak particle diameter: 24.8 ± 0.5 nm vs. 25.1 ± 0.5 nm respectively, P < 0.05). Furthermore, there was no association between the response to the OGTT and any of the apoC-III gene variants (SstI, T-455C, or C-482T) examined. Results of the present study support the notion of a hypertriglyceridemic effect associated with the apoC-III SstI polymorphism that could modulate the magnitude of the dyslipidemic state in abdominally obese patients. Apolipoprotein (apo) C-III, a protein produced by the liver, is an essential constituent of VLDL and HDL (1Mahley R.W. Innerarity T.L. Rall Jr., S.C. Weisgraber K.H. Plasma lipoproteins: apolipoprotein structure and function.J. Lipid Res. 1984; 25: 1277-1294Google Scholar). Considering the inhibitory effect of apoC-III on lipoprotein lipase (LPL) activity and hepatic uptake of lipoproteins (2McConathy W.J. Gesquiere J.C. Bass H. Tartar A. Fruchart J.C. Wang C.S. Inhibition of lipoprotein lipase activity by synthetic peptides of apolipoprotein C–III.J. Lipid Res. 1992; 33: 995-1003Google Scholar, 3Ginsberg H.N. Le N.A. Goldberg I.J. Gibson J.C. Rubinstein A. Wang-Iverson P. Norum R. Brown W.V. Apolipoprotein B metabolism in subjects with deficiency of apolipoproteins C-III and AI. Evidence that apolipoprotein C-III inhibits catabolism of triglyceride-rich lipoproteins by lipoprotein lipase in vivo.J. Clin. Invest. 1986; 78: 1287-1295Google Scholar), apoC-III gene variants have been proposed as being potentially responsible for the occurrence of lipoprotein-lipid profile disturbances. Accordingly, numerous polymorphisms in the apoC-III gene have been identified (4Talmud P.J. Humphries S.E. Apolipoprotein C–III gene variation and dyslipidaemia.Curr. Opin. Lipidol. 1997; 8: 154-158Google Scholar). The first one reported involves the substitution of a cytosine to a guanine in the 3′ untranslated region of the gene, which alters a SstI restriction site (5Rees A. Shoulders C.C. Stocks J. Galton D.J. Baralle F.E. DNA polymorphism adjacent to human apoprotein A-1 gene: relation to hypertriglyceridaemia.Lancet. 1983; 1: 444-446Google Scholar). The prevalence of the rare S2 allele in the white population has been estimated to vary between 0.08 and 0.30 (6Salas J. Jansen S. Lopez-Miranda J. Ordovas J.M. Castro P. Marin C. Ostos M.A. Bravo M.D. Jimenez-Pereperez J. Blanco A. Lopez-Segura F. Perez-Jimenez F. The SstI polymorphism of the apolipoprotein C–III gene determines the insulin response to an oral-glucose-tolerance test after consumption of a diet rich in saturated fats.Am. J. Clin. Nutr. 1998; 68: 396-401Google Scholar, 7Tybjaerg-Hansen A. Nordestgaard B.G. Gerdes L.U. Faergeman O. Humphries S.E. Genetic markers in the apo AI-C-III-AIV gene cluster for combined hyperlipidemia, hypertriglyceridemia, and predisposition to atherosclerosis.Atherosclerosis. 1993; 100: 157-169Google Scholar, 8Benlian P. Boileau C. Loux N. Pastier D. Masliah J. Coulon M. Nigou M. Ragab A. Guimard J. Ruidavets J.B. Extended haplotypes and linkage disequilibrium between 11 markers at the APOA1–C3-A4 gene cluster on chromosome 11.Am. J. Hum. Genet. 1991; 48: 903-910Google Scholar, 9Xu C.F. Nanjee M.N. Savill J. Talmud P.J. Angelico F. Del Ben M. Antonini R. Mazzarella B. Miller N. Humphries S.E. Variation at the apolipoprotein (apo) AI-C-III-AIV gene cluster and apo B gene loci is associated with lipoprotein and apolipoprotein levels in Italian children.Am. J. Hum. Genet. 1990; 47: 429-439Google Scholar, 10Ordovas J.M. Civeira F. Genest Jr., J. Craig S. Robbins A.H. Meade T. Pocovi M. Frossard P.M. Masharani U. Wilson P.W. Salem D.N. Ward R.H. Schaefer E.J. Restriction fragment length polymorphisms of the apolipoprotein A-I, C-III, A-IV gene locus. Relationships with lipids, apolipoproteins, and premature coronary artery disease.Atherosclerosis. 1991; 87: 75-86Google Scholar). The SstI apoC-III gene polymorphism has been associated with altered plasma triglyceride (TG) concentrations (4Talmud P.J. Humphries S.E. Apolipoprotein C–III gene variation and dyslipidaemia.Curr. Opin. Lipidol. 1997; 8: 154-158Google Scholar, 5Rees A. Shoulders C.C. Stocks J. Galton D.J. Baralle F.E. DNA polymorphism adjacent to human apoprotein A-1 gene: relation to hypertriglyceridaemia.Lancet. 1983; 1: 444-446Google Scholar, 7Tybjaerg-Hansen A. Nordestgaard B.G. Gerdes L.U. Faergeman O. Humphries S.E. Genetic markers in the apo AI-C-III-AIV gene cluster for combined hyperlipidemia, hypertriglyceridemia, and predisposition to atherosclerosis.Atherosclerosis. 1993; 100: 157-169Google Scholar, 10Ordovas J.M. Civeira F. Genest Jr., J. Craig S. Robbins A.H. Meade T. Pocovi M. Frossard P.M. Masharani U. Wilson P.W. Salem D.N. Ward R.H. Schaefer E.J. Restriction fragment length polymorphisms of the apolipoprotein A-I, C-III, A-IV gene locus. Relationships with lipids, apolipoproteins, and premature coronary artery disease.Atherosclerosis. 1991; 87: 75-86Google Scholar, 11Humphries S.E. Peacock R.E. Talmud P.J. The genetic determinants of plasma cholesterol and response to diet.in: Betteridge J.B. Clinical Endocrinology and Metabolism: International Practice and Research. Baillère Tindall, London1995: 797-824Google Scholar, 12Tas S. Abdella N.A. Blood pressure, coronary artery disease, and glycaemic control in type 2 diabetes mellitus: relation to apolipoprotein-C-III gene polymorphism.Lancet. 1994; 343: 1194-1195Google Scholar, 13Hoffer M.J. Sijbrands E.J. De Man F.H. Havekes L.M. Smelt A.H. Frants R.R. Increased risk for endogenous hypertriglyceridaemia is associated with an apolipoprotein C3 haplotype specified by the SstI polymorphism.Eur. J. Clin. Invest. 1998; 28: 807-812Google Scholar, 14Shoulders C.C. Grantham T.T. North J.D. Gaspardone A. Tomai F. de Fazio A. Versaci F. Gioffre P.A. Cox N.J. Hypertriglyceridemia and the apolipoprotein C-III gene locus: lack of association with the variant insulin response element in Italian school children.Hum. Genet. 1996; 98: 557-566Google Scholar, 15Zeng Q. Dammerman M. Takada Y. Matsunaga A. J. apolipoprotein C-III associated with in increased risk in a Genet. Scholar, J. of a DNA polymorphism in the apolipoprotein C–III gene with Genet. Scholar, T. M. DNA polymorphisms of apolipoprotein and insulin in and coronary disease.Atherosclerosis. Scholar, M. de Apolipoprotein gene cluster in combined effects on and apolipoproteins B and Lipid Res. 1996; Scholar, M. apolipoprotein C-III haplotype is specified by and 3′ untranslated region 1993; Scholar, J. J. Humphries S.E. Talmud P. gene variants modulate response to glucose and tolerance Scholar). the by which genetic variation to an of TG metabolism to the SstI, variations in the region of the apoC-III gene the and variants within an insulin response element of the apoC-III gene Dammerman J.D. S. T. genetic variation in the of the human apo C-III gene by insulin and to Clin. Invest. Scholar). apoC-III polymorphisms have been to a between and Dammerman J.D. S. T. genetic variation in the of the human apo C-III gene by insulin and to Clin. Invest. Scholar), and in linkage disequilibrium with the apoC-III SstI polymorphism markers in apolipoprotein C–III gene and 1996; Scholar). variation at the has been to the glucose and insulin response to an oral glucose tolerance test of the rare allele glucose and insulin concentrations the glucose J. J. Humphries S.E. Talmud P. gene variants modulate response to glucose and tolerance Scholar). Abdominal in the presence of an visceral adipose tissue (AT) has been associated with numerous metabolic that to the risk of coronary P Abdominal and an of 1992; Scholar, A.H. and 1994; Scholar, B. of diet and activity on and for the of Res. 1993; Scholar). viscerally obese subjects characterized by fasting TG and low HDL cholesterol concentrations, and insulin levels, as as by LDL particles B. of diet and activity on and for the of Res. 1993; Scholar, A. C. B. A. N. J. D. D. A. of the atherogenic metabolic in Scholar, A. B. D. A. S. F. P.J. The LDL with plasma lipoprotein levels, visceral and in 1996; Scholar). cluster of metabolic has been as the insulin is the effect of apoC-III gene polymorphisms in the viscerally obese the present study was in to the association between the apoC-III SstI, T-455C, and polymorphisms and fasting metabolic profile as as response to an OGTT in a of viscerally obese and men (mean ± SD: ± with an visceral AT area ≥130 were the and to in the which was by the of were and with or were the of the subjects was on to insulin or plasma lipoprotein and as as and were J.C. for the of visceral a J. 1993; Scholar), and the was was by the and of and Scholar). The of was in the of the of The of the Scholar). was obtained by by Abdominal visceral and AT were by which was on a D. A. C. of accumulation in J. Clin. Nutr. 1991; Scholar, M. A. S. A. S. P.J. C. of adipose tissue by in obese association with and J. Nutr. Scholar). was in and at DNA was by a of with fragment length by Dammerman M. apolipoprotein C-III haplotype is specified by and 3′ untranslated region 1993; was to the apoC-III gene were with of SstI for a of at The were to by on The the restriction site were as the SstI site were as and variations were by the as M. apolipoprotein C-III haplotype is specified by and 3′ untranslated region 1993; Scholar). Blood were obtained in the after a and TG levels were in plasma and in lipoprotein by a as S. A. F. P.J. D. C. M. A. in plasma lipoprotein in men with Scholar). Plasma < were by and the HDL obtained after of LDL in the with and M. J. cholesterol Scholar). The cholesterol and TG of the were and after the The cholesterol of and was after of with Miller M. S. and of of human plasma lipoproteins by a Lipid Res. Scholar). was in plasma by the of of by in Scholar), as P. apolipoproteins for 1: Scholar). The for were in and with obtained the for Plasma apoC-III concentrations were by human apoC-III and of variation for were LDL particle was by as A. B. D. A. S. F. P.J. The LDL with plasma lipoprotein levels, visceral and in 1996; Scholar, C. A. N. D. J. A. C. P. J. The LDL as a of in Scholar). and hepatic lipase were on one in subjects after a after an of The were a of the of and P. R. for lipoprotein lipase and hepatic lipase of H. of Scholar), as J. S. P.J. D. The relation of plasma apolipoprotein and lipoprotein cholesterol to lipoprotein lipase activity is on 1996; Scholar), and as of of plasma 75 g OGTT was in the after an Blood were a an at and for of plasma glucose and insulin Plasma glucose was R. H. Scholar), plasma insulin was by with B. of to and in Clin. 33: Scholar). Whereas the SstI polymorphism was in the and variants were in and subjects for three apoC-III gene between were for by with were for were in to study between the of glucose and insulin were by the were to the of the apoC-III gene polymorphisms, as as and metabolic to the variation in fasting plasma TG and were in and a P of was were with the the 122 subjects were obese as by a of ± and visceral accumulation as by a of ± and an visceral area of ± the of visceral AT in the 122 of the SstI, T-455C, and in the present of abdominally obese men were and Furthermore, of for variants in of men was the one by the plasma concentrations of subjects to the apoC-III polymorphisms in We found that men with the S2 allele higher fasting TG concentrations compared with S1/S1 subjects P < 0.05). with the S2 allele were characterized by LDL cholesterol and cholesterol levels, as as higher VLDL and HDL TG concentrations compared with S1/S1 subjects 2 metabolic abdominally obese men to the apoC-III gene apoC-III levels were higher in the S2 allele the was = Furthermore, no was found in plasma activity between of S2 allele were characterized by activity compared with S1/S1 subjects < 0.05). obese men the S2 allele a LDL peak particle < compared with the apoC-III SstI plasma concentrations of the subjects to the apoC-III gene of ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± of ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± of ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± as ± were in a metabolic of the subjects to the apoC-III gene of ± ± ± ± ± ± ± ± ± ± ± ± ± ± of ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± of ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± hepatic lipoprotein as ± in a as ± were hepatic lipoprotein as ± the the variants within the of the apoC-III gene to be related to lipoprotein-lipid or metabolic profile with the of a for LDL particles in of the or Furthermore, of the presence of the or only men the SstI polymorphism were fasting plasma TG the were in to the of the apoC-III gene polymorphisms and or metabolic to the in fasting plasma TG concentrations apoC-III gene polymorphism, and AT were in the the SstI polymorphism was the P < of fasting plasma TG P < to the of fasting plasma TG the metabolic were in the fasting apoC-III P < by the of fasting plasma P < and P < the of fasting plasma TG the SstI polymorphism was no a of the of plasma TG P = the of and metabolic to fasting plasma triglyceride 2 2 adipose apoC-III SstI, T-455C, and and visceral and 2 of as as fasting insulin and and in a adipose apoC-III SstI, T-455C, and and visceral and 2 of as as fasting insulin and and the presence of the apoC-III SstI polymorphism was associated with increased fasting TG levels, were in effect on the between fasting and metabolic S1/S1 TG levels were associated with a accumulation of in the as by the with = P < and visceral AT accumulation = P < 0.05). these were in men with the S2 to which was with TG in S1/S1 subjects TG levels were associated with HDL cholesterol and higher apoC-III concentrations, and an increased cholesterol as as smaller, denser LDL particles of the presence or of the S2 subjects were of the or polymorphisms, were found between fasting plasma TG and metabolic with We in the of were that the were between of the apoC-III gene with the of the of TG HDL cholesterol in S1/S1 S1/S2 between and metabolic in of apoC-III gene (n = (n = < < < < < < < < particle < < < < (n = (n = < < < < < < particle < < < < (n = (n = < < < < < particle < < < < P < P < P < in a the insulin and glucose responses to a 75 g OGTT in abdominally obese men on the of the three apoC-III gene polymorphisms We any between of the T-455C, or variants in glucose or insulin concentrations or the glucose Genetic variation in the apoC-III gene has been associated with fasting and responses to oral and glucose tolerance (4Talmud P.J. Humphries S.E. Apolipoprotein C–III gene variation and dyslipidaemia.Curr. Opin. Lipidol. 1997; 8: 154-158Google Scholar, J. Jansen S. Lopez-Miranda J. Ordovas J.M. Castro P. Marin C. Ostos M.A. Bravo M.D. Jimenez-Pereperez J. Blanco A. Lopez-Segura F. Perez-Jimenez F. The SstI polymorphism of the apolipoprotein C–III gene determines the insulin response to an oral-glucose-tolerance test after consumption of a diet rich in saturated fats.Am. J. Clin. Nutr. 1998; 68: 396-401Google Scholar, 11Humphries S.E. Peacock R.E. Talmud P.J. The genetic determinants of plasma cholesterol and response to diet.in: Betteridge J.B. Clinical Endocrinology and Metabolism: International Practice and Research. Baillère Tindall, London1995: 797-824Google Scholar, J. J. Humphries S.E. Talmud P. gene variants modulate response to glucose and tolerance Scholar). Abdominal in the presence of an increased visceral AT has been associated with in the fasting plasma lipoprotein-lipid profile that TG and levels and low HDL cholesterol concentrations, as as an increased of LDL particles B. of diet and activity on and for the of Res. 1993; Scholar, A. C. B. A. N. J. D. D. A. of the atherogenic metabolic in Scholar, A. B. D. A. S. F. P.J. The LDL with plasma lipoprotein levels, visceral and in 1996; Scholar). no study has the of the apoC-III gene variants in subjects to higher TG concentrations and insulin as viscerally obese B. of diet and activity on and for the of Res. 1993; Scholar, A. C. B. A. N. J. D. D. A. of the atherogenic metabolic in Scholar). of the variants of the apoC-III gene in the present study was to the prevalence reported in the greater area C. S. J. F. J. P. of the and SstI allele in the population of J. and M.J. Sijbrands E.J. De Man F.H. Havekes L.M. Smelt A.H. Frants R.R. Increased risk for endogenous hypertriglyceridaemia is associated with an apolipoprotein C3 haplotype specified by the SstI polymorphism.Eur. J. Clin. Invest. 1998; 28: 807-812Google Scholar, J. J. Humphries S.E. Talmud P. gene variants modulate response to glucose and tolerance Scholar), which that is that there is an increased prevalence of of the apoC-III SstI, T-455C, or variations subjects with visceral AT accumulation compared with nonobese apoC-III gene polymorphisms in the present only the SstI variant to be associated with plasma TG Indeed, found that the of the S2 allele were characterized by higher TG concentrations compared with S1/S1 the association between and the apoC-III SstI polymorphism (4Talmud P.J. Humphries S.E. Apolipoprotein C–III gene variation and dyslipidaemia.Curr. Opin. Lipidol. 1997; 8: 154-158Google Scholar, 11Humphries S.E. Peacock R.E. Talmud P.J. The genetic determinants of plasma cholesterol and response to diet.in: Betteridge J.B. Clinical Endocrinology and Metabolism: International Practice and Research. Baillère Tindall, London1995: 797-824Google Scholar). found of the presence or of the SstI polymorphism, viscerally obese subjects were characterized by fasting TG Indeed, of subjects TG levels an to TG concentrations as by the on and Genest Jr., for the and of of the on and J. Scholar). that the hypertriglyceridemic state that visceral B. of diet and activity on and for the of Res. 1993; Scholar, A. C. B. A. N. J. D. D. A. of the atherogenic metabolic in results a greater of S1/S2 in the viscerally obese The SstI site could be in linkage disequilibrium with that apoC-III has been that in the of the apoC-III gene have a association with the SstI polymorphism M. apolipoprotein C-III haplotype is specified by and 3′ untranslated region 1993; Scholar). results that linkage disequilibrium between the SstI polymorphism and these apoC-III gene variants C.C. Grantham T.T. North J.D. Gaspardone A. Tomai F. de Fazio A. Versaci F. Gioffre P.A. Cox N.J. Hypertriglyceridemia and the apolipoprotein C-III gene locus: lack of association with the variant insulin response element in Italian school children.Hum. Genet. 1996; 98: 557-566Google Scholar, markers in apolipoprotein C–III gene and 1996; the association between TG levels and the S2 Indeed, markers in apolipoprotein C–III gene and 1996; the of C-482T, and were in linkage disequilibrium with and with the S2 were to an association of any S2 haplotype with levels of plasma and by the presence of the S2 is with results no of the and polymorphisms to fasting plasma TG Furthermore, in men the or only the S2 allele TG levels the the a association has been reported between the SstI site and variants within the apoC-III gene C.F. Talmud P. Humphries S. polymorphisms of the gene 1994; 8: Scholar). no study has a between these and any of apoC-III that could the proposed association between and We the of linkage disequilibrium with variants in the apoC-III variants in the gene M. J.C. Cox Fruchart J.C. apolipoprotein in and by the apoC-III gene to be investigated and be as a in the association between higher TG and the apoC-III SstI as a effect of the SstI polymorphism on be H. F. in apolipoprotein C–III in human Scholar). apoC-III concentrations have been associated with plasma TG levels the of activity and of lipoprotein by the (2McConathy W.J. Gesquiere J.C. Bass H. Tartar A. Fruchart J.C. Wang C.S. Inhibition of lipoprotein lipase activity by synthetic peptides of apolipoprotein C–III.J. Lipid Res. 1992; 33: 995-1003Google Scholar, 3Ginsberg H.N. Le N.A. Goldberg I.J. Gibson J.C. Rubinstein A. Wang-Iverson P. Norum R. Brown W.V. Apolipoprotein B metabolism in subjects with deficiency of apolipoproteins C-III and AI. Evidence that apolipoprotein C-III inhibits catabolism of triglyceride-rich lipoproteins by lipoprotein lipase in vivo.J. Clin. Invest. 1986; 78: 1287-1295Google Scholar). is by results that that the plasma apoC-III was the of plasma TG in of Furthermore, to the between the apoC-III gene SstI polymorphism and apoC-III levels has been in viscerally obese individuals. a for higher plasma apoC-III levels was found in S1/S2 the with S1/S1 subjects ± vs. ± respectively, P = to lack of Furthermore, as only plasma apoC-III concentrations, be in to a of the SstI polymorphism to the of apoC-III in lipoprotein and which could the association between and the SstI The of of has been as and P. B. M.J. M.A. apolipoproteins C-III, and and risk of coronary in the cholesterol and that the apoC-III in in was an of coronary the the hypertriglyceridemic state of S1/S2 men compared with S1/S1 subjects be at in by the activity in the S2 allele The between activity and the TG of LDL = P < a support of S1/S2 men were characterized by higher and levels, activity compared with S1/S1 the apoC-III SstI was a of plasma activity P = The insulin response to an OGTT has been reported to be by the apoC-III gene polymorphism (6Salas J. Jansen S. Lopez-Miranda J. Ordovas J.M. Castro P. Marin C. Ostos M.A. Bravo M.D. Jimenez-Pereperez J. Blanco A. Lopez-Segura F. Perez-Jimenez F. The SstI polymorphism of the apolipoprotein C–III gene determines the insulin response to an oral-glucose-tolerance test after consumption of a diet rich in saturated fats.Am. J. Clin. Nutr. 1998; 68: 396-401Google Scholar, J. J. Humphries S.E. Talmud P. gene variants modulate response to glucose and tolerance Scholar). the present no was found in the glucose or insulin response to the glucose men the allele of the SstI, T-455C, or is that visceral is associated with in S. of visceral to the of type diabetes and for and 1994; Scholar). Whereas (6Salas J. Jansen S. Lopez-Miranda J. Ordovas J.M. Castro P. Marin C. Ostos M.A. Bravo M.D. Jimenez-Pereperez J. Blanco A. Lopez-Segura F. Perez-Jimenez F. The SstI polymorphism of the apolipoprotein C–III gene determines the insulin response to an oral-glucose-tolerance test after consumption of a diet rich in saturated fats.Am. J. Clin. Nutr. 1998; 68: 396-401Google and J. J. Humphries S.E. Talmud P. gene variants modulate response to glucose and tolerance nonobese investigated only viscerally obese in between the for the in the response to the OGTT between of the SstI, T-455C, or the of visceral on metabolism could be greater the of the apoC-III gene polymorphism to plasma results that the apoC-III SstI polymorphism is associated with in viscerally obese subjects characterized by plasma TG the between fasting TG levels and to be altered by the presence of the rare S2 and that the between TG and metabolic risk profile in S1/S1 and S1/S2 that the of higher TG levels in apoC-III SstI polymorphism to be of and that the of increased TG concentrations on HDL cholesterol levels and LDL particle is by the presence of the apoC-III SstI polymorphism, at in viscerally obese study was with the support of the of and and by the and and J.B. the de is a of the of is a of a the and of is of and by and the of the The to the of the for and the of the Lipid for and to the

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