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• W2156425270 abstract "Turks have strikingly low levels of high density lipoprotein cholesterol (HDL-C) (10–15 mg/dL lower than those of Americans or Western Europeans) associated with elevated hepatic lipase mass and activity. Here we report that Turks have low levels of high density lipoprotein subclass 2 (HDL2), apoA-I-containing lipoproteins (LpA-I), and pre-β-1 HDL and increased levels of HDL3 and LpA-I/A-II particles (potentially an atherogenic lipid profile). The frequency distributions of HDL-C and LpA-I levels were skewed toward bimodality in Turkish women but were unimodal in Turkish men. The apoE genotype affected HDL-C and LpA-I levels in women only. In women, but not men, the ε2 allele was strikingly more prevalent in those with the highest levels of HDL-C and LpA-I than in those with the lowest levels. The higher prevalence of the ε2 allele in these subgroups of women was not explained by plasma triglyceride levels, total cholesterol levels, age, or body mass index. The modulating effects of apoE isoforms on lipolytic hydrolysis of HDL by hepatic lipase (apoE2 preventing efficient hydrolysis) or on lipoprotein receptor binding (apoE2 interacting poorly with the low density lipoprotein receptors) may account for differences in HDL-C levels in Turkish women (the ε2 allele being associated with higher HDL levels). In Turkish men, who have substantially higher levels of hepatic lipase activity than women, the modulating effect of apoE may be overwhelmed. The gender-specific impact of the apoE genotype on HDL-C and LpA-I levels in association with elevated levels of hepatic lipase provides new insights into the metabolism of HDL. —Mahley, R. W., J. Pépin, K. Erhan Palaogğlu, M. J. Malloy, J. P. Kane, and T. P. Bersot. Low levels of high density lipoproteins in Turks, a population with elevated hepatic lipase: high density lipoprotein characterization and gender-specific effects of apolipoprotein E genotype. J. Lipid Res. 2000. 41: 1290–1301. Turks have strikingly low levels of high density lipoprotein cholesterol (HDL-C) (10–15 mg/dL lower than those of Americans or Western Europeans) associated with elevated hepatic lipase mass and activity. Here we report that Turks have low levels of high density lipoprotein subclass 2 (HDL2), apoA-I-containing lipoproteins (LpA-I), and pre-β-1 HDL and increased levels of HDL3 and LpA-I/A-II particles (potentially an atherogenic lipid profile). The frequency distributions of HDL-C and LpA-I levels were skewed toward bimodality in Turkish women but were unimodal in Turkish men. The apoE genotype affected HDL-C and LpA-I levels in women only. In women, but not men, the ε2 allele was strikingly more prevalent in those with the highest levels of HDL-C and LpA-I than in those with the lowest levels. The higher prevalence of the ε2 allele in these subgroups of women was not explained by plasma triglyceride levels, total cholesterol levels, age, or body mass index. The modulating effects of apoE isoforms on lipolytic hydrolysis of HDL by hepatic lipase (apoE2 preventing efficient hydrolysis) or on lipoprotein receptor binding (apoE2 interacting poorly with the low density lipoprotein receptors) may account for differences in HDL-C levels in Turkish women (the ε2 allele being associated with higher HDL levels). In Turkish men, who have substantially higher levels of hepatic lipase activity than women, the modulating effect of apoE may be overwhelmed. The gender-specific impact of the apoE genotype on HDL-C and LpA-I levels in association with elevated levels of hepatic lipase provides new insights into the metabolism of HDL. —Mahley, R. W., J. Pépin, K. Erhan Palaogğlu, M. J. Malloy, J. P. Kane, and T. P. Bersot. Low levels of high density lipoproteins in Turks, a population with elevated hepatic lipase: high density lipoprotein characterization and gender-specific effects of apolipoprotein E genotype. J. Lipid Res. 2000. 41: 1290–1301. In the United States and Western Europe, low levels of high density lipoprotein cholesterol (HDL-C), defined as HDL-C <35 mg/dL, occur in about 15% of men and 5% of women (1National Cholesterol Education Program Second report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II).Circulation. 1994; 89: 1333-1445Google Scholar). Low HDL-C is associated with an increased prevalence of premature coronary heart disease (2Schaefer E.J. Lamon-Fava S. Ordovas J.M. Cohn S.D. Schaefer M.M. Castelli W.P. Wilson P.W.F. Factors associated with low and elevated plasma high density lipoprotein cholesterol and apolipoprotein A-I levels in the Framingham Offspring Study.J. Lipid Res. 1994; 35: 871-882Google Scholar, 3Miller N.E. Førde O.H. Thelle D.S. Mjøs O.D. The Tromsø Heart-Study. High-density lipoprotein and coronary heart-disease: a prospective case-control study.Lancet. 1977; 1: 965-968Google Scholar, 4Gordon T. Castelli W.P. Hjortland M.C. Kannel W.B. Dawber T.R. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study.Am. J. Med. 1977; 62: 707-714Google Scholar, 5Genest Jr., J.J. Martin-Munley S.S. McNamara J.R. Ordovas J.M. Jenner J. Myers R.H. Silberman S.R. Wilson P.W.F. Salem D.N. Schaefer E.J. Familial lipoprotein disorders in patients with premature coronary artery disease.Circulation. 1992; 85: 2025-2033Google Scholar). HDL-C levels are influenced by a complex interaction of behavioral, metabolic, and genetic factors. Behavioral factors that impact HDL-C levels include smoking, exercise, obesity, types and amounts of dietary fat, and ethanol consumption (6Craig W.Y. Palomaki G.E. Haddow J.E. Cigarette smoking and serum lipid and lipoprotein concentrations: an analysis of published data.Br. Med. J. 1989; 298: 784-788Google Scholar, 7Denke M.A. Sempos C.T. Grundy S.M. Excess body weight. An underrecognized contributor to high blood cholesterol levels in white American men.Arch. Intern. Med. 1993; 153: 1093-1103Google Scholar, 8Denke M.A. Sempos C.T. Grundy S.M. Excess body weight. An under-recognized contributor to dyslipidemia in white American women.Arch. Intern. Med. 1994; 154: 401-410Google Scholar, 9Kris-Etherton P.M. Derr J. Mitchell D.C. Mustad V.A. Russell M.E. McDonnell E.T. Salabsky D. Pearson T.A. The role of fatty acid saturation on plasma lipids, lipoproteins, and apolipoproteins. I. Effects of whole food diets high in cocoa butter, olive oil, soybean oil, dairy butter, and milk chocolate on the plasma lipids of young men.Metabolism. 1993; 42: 121-129Google Scholar, 10Grundy S.M. Denke M.A. Dietary influences on serum lipids and lipoproteins.J. Lipid Res. 1990; 31: 1149-1172Google Scholar, 11Mattson F.H. Grundy S.M. Comparison of effects of dietary saturated, monounsaturated, and polyunsaturated fatty acids on plasma lipids and lipoproteins in man.J. Lipid Res. 1985; 26: 194-202Google Scholar, 12Mensink R.P. Katan M.B. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials.Arterioscler. Thromb. 1992; 12: 911-919Google Scholar). Metabolic and genetic factors include various primary hypertriglyceridemias, type II diabetes mellitus, isolated low HDL-C, and mutations in the genes encoding apolipoprotein A-I (apoA-I), lecithin:cholesterol acyltransferase, and cholesteryl ester transfer protein (CETP) (5Genest Jr., J.J. Martin-Munley S.S. McNamara J.R. Ordovas J.M. Jenner J. Myers R.H. Silberman S.R. Wilson P.W.F. Salem D.N. Schaefer E.J. Familial lipoprotein disorders in patients with premature coronary artery disease.Circulation. 1992; 85: 2025-2033Google Scholar, 13Vega G.L. Grundy S.M. Hypoalphalipoproteinemia (low high density lipoprotein) as a risk factor for coronary heart disease.Curr. Opin. Lipidol. 1996; 7: 209-216Google Scholar, 14Schaefer E.J. Clinical, biochemical, and genetic features in familial disorders of high density lipoprotein deficiency.Arteriosclerosis. 1984; 4: 303-322Google Scholar). Variability in the activity of hepatic triglyceride lipase (HTGL) or lipoprotein lipase (LPL) also affects HDL-C levels (13Vega G.L. Grundy S.M. Hypoalphalipoproteinemia (low high density lipoprotein) as a risk factor for coronary heart disease.Curr. Opin. Lipidol. 1996; 7: 209-216Google Scholar). The apoA-I and HTGL loci account for about one-half of the interindividual variation in HDL-C (15Cohen J.C. Wang Z. Grundy S.M. Stoesz M.R. Guerra R. Variation at the hepatic lipase and apolipoprotein AI/CIII/AIV loci is a major cause of genetically determined variation in plasma HDL cholesterol levels.J. Clin. Invest. 1994; 94: 2377-2384Google Scholar). Low HDL-C levels are more prevalent in Turkey than in any other country where plasma lipid values have been extensively characterized (16Mahley R.W. Palaoglu K.E. Atak Z. Dawson-Pepin J. Langlois A-M. Cheung V. Onat H. Fulks P. Mahley L.L. Vakar F. Özbayrakçı S. Gökdemir O. Winkler W. Turkish Heart Study: lipids, lipoproteins, and apolipoproteins.J. Lipid Res. 1995; 36: 839-859Google Scholar). Data from the Turkish Heart Study have demonstrated that 53% of men and 26% of women in Turkey have HDL-C levels below 35 mg/dL. The low HDL-C levels were found irrespective of geographic location or substantial regional variation in diet, and were not attributable to behavioral factors (smoking, exercise, or alcohol consumption) that commonly modulate HDL-C levels. Turks with low HDL-C levels do not have significantly elevated triglyceride levels, suggesting that their low HDL-C levels are predominantly an example of isolated low HDL-C (16Mahley R.W. Palaoglu K.E. Atak Z. Dawson-Pepin J. Langlois A-M. Cheung V. Onat H. Fulks P. Mahley L.L. Vakar F. Özbayrakçı S. Gökdemir O. Winkler W. Turkish Heart Study: lipids, lipoproteins, and apolipoproteins.J. Lipid Res. 1995; 36: 839-859Google Scholar). These observations have been confirmed and extended by Onat et al. (17Onat A. Büyükbese M.A. Ural E. Keles I. Ural D. Ince E. Kurban B. Sansoy V. Marmara bölgesi halkında HDL-kolesterol ile fibrinojen düzeyleri ve bazı etkenlerle iliskileri.Arch. Turk. Soc. Cardiol. 1997; 25: 520-525Google Scholar) and Hergenç et al. (18Hergenç G. Schulte H. Assmann G. von Eckardstein A. Associations of obesity markers, insulin, and sex hormones with HDL-cholesterol levels in Turkish and German individuals.Atherosclerosis. 1999; 145: 147-156Google Scholar). In our study to determine the cause of low HDL-C in the Turkish population, the activities of HTGL, LPL, CETP, and lecithin:cholesterol acyltransferase were measured in Turkish men and women residing in Istanbul and compared with the values in non-Turkish control subjects residing in San Francisco (19Bersot T.P. Vega G.L. Grundy S.M. Palaoglu K.E. Atagündüz P. Özbayrakçi S. Gökdemir O. Mahley R.W. Elevated hepatic lipase activity and low levels of high density lipoprotein in a normotriglyceridemic, nonobese Turkish population.J. Lipid Res. 1999; 40: 432-438Google Scholar). In normotriglyceridemic, nonobese subjects, the most striking finding was the elevated HTGL activity in Turkish men and women with reduced mean HDL-C levels (men, 37 mg/dL; women, 43 mg/dL). The mean HTGL activities were 24 and 31% higher in Turkish men and women, respectively, than in age- and sex-matched white Americans with higher mean HDL-C levels (men, 47 mg/dL; women, 58 mg/dL). Elevated HTGL activity is associated with low levels of plasma HDL (13Vega G.L. Grundy S.M. Hypoalphalipoproteinemia (low high density lipoprotein) as a risk factor for coronary heart disease.Curr. Opin. Lipidol. 1996; 7: 209-216Google Scholar). In the present study, we characterized in detail the subclasses of plasma HDL in 406 Turkish men and women residing in Istanbul. The HDL were separated into apolipoprotein A-I-containing lipoproteins (LpA-I) and LpA-I/A-II subclasses and HDL subclass 2 (HDL2) and HDL3. The concentration of pre-β-1 HDL was also determined. Anthropometric data, plasma lipid and lipoprotein cholesterol levels, apoA-I levels, and apoE genotypes were also measured to assess their relationships to the concentrations of the HDL subclasses. Healthy Turkish volunteers who were employees, or relatives or friends of employees, of the Koç American Hospital in Istanbul were recruited for the study. Subjects with acute or chronic medical problems and those using hypolipidemic drugs, hormone replacement, oral contraceptives, β-blockers, and thiazide diuretics were excluded. There were 196 male and 210 female adult volunteers. The characteristics of the study population are summarized in Table 1.TABLE 1.Characteristics of Istanbul men and womenAgeBMITCTC >240 mg/dLLDL-CLDL-C >160 mg/dLHDL-CHDL-C ≤35 mg/dLHDL-C >45 mg/dLTGTG >200 mg/dLTC/HDL-CTC/HDL-C >4.5TC/HDL-C >5.5Mean ± SDMean ± SDmg/dL, mean ± SD%mg/dL, mean ± SD%mg/dL ± SD%%mg/dL ± SD%Mean ± SD%%Men (n = 196)42 ± 1227 ± 4197 ± 4616126 ± 381736 ± 8569174 ± 106275.7 ± 1.87248Women (n = 210)40 ± 1226 ± 5191 ± 5016126 ± 421842 ± 92628118 ± 68154.8 ± 1.64826BMI, body mass index; TC, total cholesterol; LDL-C, low density lipoprotein cholesterol; HDL-C, high density lipoprotein cholesterol; TG, triglycerides. Open table in a new tab BMI, body mass index; TC, total cholesterol; LDL-C, low density lipoprotein cholesterol; HDL-C, high density lipoprotein cholesterol; TG, triglycerides. The study protocol was approved by the Committee on Human Research of the University of California, San Francisco, and all participants gave informed consent. All subjects fasted for 12 h before blood was drawn for measurement of plasma lipids and lipoproteins. To prevent coagulation and reduce the possibility of sample degradation before the assay, 10 μL of a solution containing ethylenediaminetetraacetic acid (EDTA; final concentration, 1 mg/mL), chloramphenicol (0.005%), gentamicin sulfate (0.005%), sodium azide (0.01%), and aprotinin (100 IU/mL) was added to each tube. Blood was drawn into precooled tubes and immediately placed on ice. Plasma was separated from the cells within 2 h. Aliquots for the various assays were frozen at −70°C. The plasma cholesterol, plasma triglyceride, and HDL-C concentrations were measured by enzymatic techniques in the lipid diagnostic laboratory of the Koç American Hospital. This laboratory has been certified as a lipid reference laboratory by the Centersfor Disease Control (16Mahley R.W. Palaoglu K.E. Atak Z. Dawson-Pepin J. Langlois A-M. Cheung V. Onat H. Fulks P. Mahley L.L. Vakar F. Özbayrakçı S. Gökdemir O. Winkler W. Turkish Heart Study: lipids, lipoproteins, and apolipoproteins.J. Lipid Res. 1995; 36: 839-859Google Scholar). HDL-C levels were measured after very low density lipoproteins (VLDL) and low density lipoproteins (LDL) were precipitated with phosphotungstic acid and magnesium. Kits for the lipid assays were from Boehringer Mannheim (Mannheim, Germany). A Hitachi (Tokyo, Japan) multichannel analyzer was used for the colorometric enzymatic determinations (Monotest Cholesterol, CHOD-PAP; Peridochrom Triglyceride, GPO-PAP). The Friedewald calculation was used to estimate LDL-C values (20Friedewald W.T. Levy R.I. Fredrickson D.S. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge.Clin. Chem. 1972; 18: 499-502Google Scholar). Apolipoprotein E phenotyping was performed as described previously (16Mahley R.W. Palaoglu K.E. Atak Z. Dawson-Pepin J. Langlois A-M. Cheung V. Onat H. Fulks P. Mahley L.L. Vakar F. Özbayrakçı S. Gökdemir O. Winkler W. Turkish Heart Study: lipids, lipoproteins, and apolipoproteins.J. Lipid Res. 1995; 36: 839-859Google Scholar). LpA-I were analyzed with an electroimmunoassay based on a previously described immunoassay that had intra- and interassay variations of less than 5% (21Parra H.J. Mezdour H. Ghalim N. Bard J.M. Fruchart J.C. Differential electroimmunoassay of human LpA-I lipoprotein particles on ready-to-use plates.Clin. Chem. 1990; 36: 1431-1435Google Scholar). Total apoA-I was measured from whole plasma with Hydragel apoA-I/B kits (Sebia, Norcross, GA). Plasma was prestained with Sudan black, diluted with the EID buffer provided in the kit, and loaded onto ready-made agarose gels into which monospecific antibodies against apoA-I and apoB had been incorporated. The antibody concentrations were adjusted to produce two rockets on the gels during electrophoresis, one corresponding to apoB and one to apoA-I. Gels were electrophoresed for 3.5 h at 100 V, washed in 0.15 m saline, and dried, and the apoA-I rocket was measured to the nearest half-millimeter. A standard curve was calculated for every gel from standard serum provided in the kit, and sample apoA-I concentrations were calculated from the curve. A control plasma sample was included on every gel. The HDL2 and HDL3 were isolated by double precipitation as described by Gidez et al. (22Gidez L.I. Miller G.J. Burstein M. Slagle S. Eder H.A. Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure.J. Lipid Res. 1982; 23: 1206-1223Google Scholar). All apoB-containing lipoproteins were precipitated by mixing 1 mL of plasma with 0.1 mL of heparin–MnCl2. Heparin sodium salt (157 USP units/mg dry weight) and manganese chloride (MnCl2·4H2O) were obtained from Sigma (St. Louis, MO). The samples were mixed thoroughly, allowed to stand at room temperature for 15 min, and centrifuged at 2,500 rpm for 1 h at 4°C. The supernatant (HDL) was removed. An aliquot was reserved for cholesterol analysis, and the remainder was used to isolate HDL3. HDL2 were precipitated by adding 0.06 mL of dextran sulfate solution (14.3 mg/dL in 0.15 m NaCl) to 0.6 mL of the heparin – MnCl2 supernatant. Dextran sulfate (molecular weight 1,500, Dextralip 15) was purchased from Genzyme Diagnostics (Cambridge, MA). The samples were mixed thoroughly by vortexing, incubated at room temperature for 20 min, and centrifuged at 2,500 rpm for 30 min at 4°C. The supernatant (HDL3) was removed and reserved for cholesterol analysis. Total HDL-C and HDL3-C in each sample were measured in the same assay with CHOL kits (Boehringer Mannheim) that utilize the CHOD-PAP method. Spectrum system cholesterol standards from Abbott Laboratories (Chicago, IL) were used to calculate a standard curve for each assay. HDL2-C was calculated as the difference between total HDL-C and HDL3-C. Pre-β-1 HDL were measured with an isotope dilution assay (23O'Connor P.M. Zysow B.R. Schoenhaus S.A. Ishida B.Y. Kunitake S.T. Naya-Vigne J.M. Duchateau P.N. Redberg R.F. Spencer S.J. Mark S. Mazur M. Heilbron D.C. Jaffe R.B. Malloy M.J. Kane J.P. Prebeta-1 HDL in plasma of normolipidemic individuals: influences of plasma lipoproteins, age, and gender.J. Lipid Res. 1998; 39: 670-678Google Scholar, 24O'Connor P.M. Naya-Vigne J.M. Duchateau P.N. Ishida B.Y. Mazur M. Schoenhaus S.A. Zysow B.R. Malloy M.J. Kunitake S.T. Kane J.P. Measurement of prebeta-1 HDL in human plasma by an ultrafiltration-isotope dilution technique.Anal. Biochem. 1997; 251: 234-240Google Scholar). Total LpA-I was obtained from plasma samples by selective affinity immunosorption, and pre-β-1 HDL were isolated by starch block electrophoresis. The pre-β-1 HDL used for the dilution probe were labeled with tritium and added to the plasma samples. The plasma samples were ultrafiltered at a cutoff of 100 kDa to separate the pre-β-1 HDL from other apoA-I-containing lipoproteins. The specific activity of the ultrafiltrate was determined by scintillation counting, and the apoA-I levels in the plasma and ultrafiltrate were measured by an enzyme-linked immunosorbent assay technique. The amount of pre-β-1 HDL in the plasma was calculated by the isotope dilution equation. Group means (results listed in the tables) were compared by two-sample t-tests. A probability value of 0.05 or less was considered significant. Relationships between the ε2 allele and levels of HDL-C and LpA-I were assessed by chi-square analysis. Microsoft (Redmond, WA) Excel 5.0 for the Macintosh was used for data management and statistical analyses. The study population consisted of 196 Turkish men and 210 Turkish women from Istanbul (Table 1). The men and women were of a similar age and body mass index (BMI) and had similar total cholesterol (~195 mg/dL) and LDL-C (126 mg/dL) levels. In agreement with previous observations (16Mahley R.W. Palaoglu K.E. Atak Z. Dawson-Pepin J. Langlois A-M. Cheung V. Onat H. Fulks P. Mahley L.L. Vakar F. Özbayrakçı S. Gökdemir O. Winkler W. Turkish Heart Study: lipids, lipoproteins, and apolipoproteins.J. Lipid Res. 1995; 36: 839-859Google Scholar), the mean HDL-C levels were 10–15 mg/dL lower in both Turkish men and women (36 and 42 mg/dL, respectively) than in U.S. or Western European populations, and ~56% of the men and 26% of the women had HDL-C levels <35 mg/dL. As a result, the mean total cholesterol/HDL-C ratios were markedly higher in Turks than in U.S. subjects (men, 5.7 vs. 4.5; women, 4.8 vs. 3.8) (25Johnson C.L. Rifkind B.M. Sempos C.T. Carroll M.D. Bachorik P.S. Briefel R.R. Gordon D.J. Burt V.L. Brown C.D. Lippel K. Cleeman J.I. Declining serum total cholesterol levels among US adults. The National Health and Nutrition Examination Surveys.J. Am. Med. Assoc. 1993; 269: 3002-3008Google Scholar). Cholesterol/HDL-C ratios were >4.5 in 70% of Turkish men and 50% of Turkish women, and >5.5 in 48% of the men and 26% of the women. Mean triglyceride levels were higher in men than in women, but were below 175 mg/dL in both groups. Analysis of the frequency distribution of HDL-C levels (Fig. 1) showed a skewed distribution in Turkish women (a peak at 39 mg/dL and a major shoulder between 44 and 54 mg/dL) and a unimodal distribution without skewedness in men (a peak at 34 mg/dL). In white American men, the unimodal HDL-C distribution, based on NHANES (National Health and Nutrition Examination Surveys) data, peaked at 40–45 mg/dL (26Carroll M. Sempos C. Briefel R. Gray S. Johnson C. Serum Lipids of Adults 20–74 Years: United States, 1976–80.Vital and Health Statistics. Series 11: Data from the National Health Survey No. 242. National Center for Health Statistics, U.S. Department of Health and Human Services, Hyattsville, MD1993Google Scholar). In Americanwomen, the HDL-C distribution was also skewed with a peak at ~50 mg/dL and a shoulder at 64 to 74 mg/dL (26Carroll M. Sempos C. Briefel R. Gray S. Johnson C. Serum Lipids of Adults 20–74 Years: United States, 1976–80.Vital and Health Statistics. Series 11: Data from the National Health Survey No. 242. National Center for Health Statistics, U.S. Department of Health and Human Services, Hyattsville, MD1993Google Scholar). The HDL in Turks were characterized by electroimmunoassay to measure LpA-I and LpA-I/A-II and by heparin–manganese precipitation to measure HDL2 and HDL3. The plasma apoA-I, LpA-I, and LpA-I/A-II concentrations for Turkish subjects were compared with previously published data from French men and women and American men with normal HDL-C or low HDL-C levels (Table 2). Even though the HDL-C values were 20 mg/dL higher in French and American subjects than in Turks, the plasma total apoA-I levels were similar (~120–130 mg/dL). However, the Turks had significantly lower LpA-I and higher LpA-I/A-II levels. The ratio of LpA-I to LpA-I/A-II was 0.51 for Turkish men and 0.69 for Turkish women compared with 0.69–0.75 for French and American men and 0.82 for French women. Even in the American men with low HDL-C levels, similar to the typical levels in Turkish men, the LpA-I:LpA-I/A-II ratio was 0.70. The LpA-I accounted for 41–45% of the total plasma apoA-I in non-Turks and 31–38% in the Turks (Table 2).TABLE 2.Concentration of lipids (mean mg/dL ± SD), apoA-I, LpA-I, and LpA-I/AII (mean mg apoA-I/dL ± SD), and ratio of LpA-I:LpA-I/A-II (mean ± SD) for normolipidemic subjects of Turkish, French, and American originApoA-InCholesterolHDL-CTotal ApoA-ILpA-ILpA-I/A-IILpA-I: LpA-I/A-IITurkishMen196197 ± 4636 ± 8122 ± 1939 ± 9 (31%)aData adapted from ref. 21.84 ± 180.51 ± 0.38Women210191 ± 5042 ± 9123 ± 1948 ± 13 (38%)aData adapted from ref. 21.76 ± 180.69 ± 0.33FrenchbLpA-I as a percentage of total plasma apoA-I.Men40224 ± 3459 ± 15120 ± 2049 ± 9 (41%)aData adapted from ref. 21.71cCalculated (mean total apoA-I - mean apoA-I in LpA-I).0.69dCalculated (mean apoA-I in LpA-I ÷ mean apoA-I in LpA-I/A-II).Women45208 ± 3665 ± 14133 ± 1760 ± 13 (45%)aData adapted from ref. 21.73cCalculated (mean total apoA-I - mean apoA-I in LpA-I).0.82dCalculated (mean apoA-I in LpA-I ÷ mean apoA-I in LpA-I/A-II).AmericaneFrom ref. 53; reported as mean ± SEM.Men27204 ± 553 ± 2123 ± 453 ± 1 (43%)aData adapted from ref. 21.70 ± 30.75MenfA low HDL-C subgroup of American men from ref. 53.49188 ± 334 ± 1102 ± 342 ± 1 (41%)aData adapted from ref. 21.60 ± 30.70a Data adapted from ref. 21Parra H.J. Mezdour H. Ghalim N. Bard J.M. Fruchart J.C. Differential electroimmunoassay of human LpA-I lipoprotein particles on ready-to-use plates.Clin. Chem. 1990; 36: 1431-1435Google Scholar.b LpA-I as a percentage of total plasma apoA-I.c Calculated (mean total apoA-I - mean apoA-I in LpA-I).d Calculated (mean apoA-I in LpA-I ÷ mean apoA-I in LpA-I/A-II).e From ref. 53Montali A. Vega G.L. Grundy S.M. Concentrations of apolipoprotein A-I-containing particles in patients with hypoalphalipoproteinemia.Arterioscler. Thromb. 1994; 14: 511-517Google Scholar; reported as mean ± SEM.f A low HDL-C subgroup of American men from ref. 53Montali A. Vega G.L. Grundy S.M. Concentrations of apolipoprotein A-I-containing particles in patients with hypoalphalipoproteinemia.Arterioscler. Thromb. 1994; 14: 511-517Google Scholar. Open table in a new tab The frequency distributions of LpA-I levels in Turkish men and women were similar to those of HDL-C levels (Fig. 2). Among men, the distribution was unimodal, with a peak at 40 mg of apoA-I/dL in the LpA-I class. Among women, LpA-I levels peaked at 48 mg/dL, with a shoulder at ~60–70 mg/dL. For approximately one-fourth of Turkish subjects (selected at random), HDL2-C and HDL3-C values were compared with LpA-I and LpA-I/A-II values (Table 3). In men and women, ~30–40% of the HDL-C and apoA-I occurred in HDL2 and LpA-I, respectively, with the remainder in HDL3 and LpA-I/A-II. LpA-I corresponds roughly to HDL2 and LpA-I/A-II to HDL3 (27Cheung M.C. Albers J.J. Characterization of lipoprotein particles isolated by immunoaffinity chromatography. Particles containing A-I and A-II and particles containing A-I but no A-II.J. Biol. Chem. 1984; 259: 12201-12209Google Scholar, 28Nestruck A.C. Niedmann P.D. Wieland H. Seidel D. Chromatofocusing of human high density lipoproteins and isolation of lipoproteins A and A-I.Biochim. Biophys. Acta. 1983; 753: 65-73Google Scholar, 29von Eckardstein A. Huang Y. Assmann G. Physiological role and clinical relevance of high-density lipoprotein subclasses.Curr. Opin. Lipidol. 1994; 5: 404-416Google Scholar). HDL2 and LpA-I levels were lower in subjects with low HDL-C (≤35 mg/dL in men; ≤40 mg/dL in women); the difference was especially marked in the women (Table 3). Thus, the low HDL-C levels in Turks were primarily accounted for by reductions in HDL2-C and LpA-I levels and a relative increase in HDL3-C and LpA-I/A-II levels (TABLE 2., TABLE 3.).TABLE 3.HDL-C subclasses and LpA-I and LpA-I/A-II valuesnHDL-C (ppt)aHDL-C determined on fractions after heparin-manganese precipitation.HDL2-C (ppt)aHDL-C determined on fractions after heparin-manganese precipitation.HDL3-C (ppt)aHDL-C determined on fractions after heparin-manganese precipitation.HDL2HDL3LpA-ILpA-I/A-IImg/dL% total HDL-C% total apoA-ITurkish men5138 ± 912 ± 726 + 631693070Turkish women4948 ± 1318 ± 1030 ± 635654060Turkish menHDL-C ≤35 mg/dL2633 ± 6bP < 0.01.10 ± 523 ± 430702971HDL-C >35 mg/dL2543 ± 9bP < 0.01.14 ± 828 ± 632683268Turkish womenHDL-C ≤40 mg/dL2137 ± 7cP < 0.001.10 ± 6dP < 0.005.27 ± 427733466HDL-C >40 mg/dL2857 ± 10cP < 0.001.23 ± 8dP < 0.005.33 ± 741594555a HDL-C determined on fractions after heparin-manganese precipitation.b P < 0.01.c P < 0.001.d P < 0.005. Open table in a new tab In a subset of Turks, pre-β-1 HDL (the precursor of HDL) values were compared with those of non-Turkish American control subjects living in San Francisco (23O'Connor P.M. Zysow B.R. Schoenhaus S.A. Ishida B.Y. Kunitake S.T. Naya-Vigne J.M. Duchateau P.N. Redberg R.F. Spencer S.J. Mark S. Mazur M. Heilbron D.C. Jaffe R.B. Malloy M.J. Kane J.P. Prebeta-1 HDL in plasma of normolipidemic individuals: influences of plasma lipoproteins, age, and gender.J. Lipid Res. 1998; 39: 670-678Google Scholar). In Turks, the pre-β-1 HDL levels were approximately 40% lower than in the controls, and the apoA-I levels were about 10–15% lower (Table 4). Thus, Turks tend to have decreases not only in LpA-I and HDL2, but also in pre-β-1 HDL precursors.TABLE 4.Pre-β-1 HDL levels in Americans and TurksnPre-β-1HDL-CApoA-ICholesterolTriglyceridesμg/mL apoA-Img/dLMenSan FranciscoaData from O'Connor et al. (23).4684 ± 49bP < 0.03.48 ± 11116 ± 27175 ± 2881 ± 27Turkish1752 ± 28bP < 0.03.37 ± 7108 ± 17169 ± 45112 ± 33WomenSan FranciscoaData from O'Connor et al. (23).9068 ± 40cP < 0.02.58 ± 12125 ± 31179 ± 2977 ± 23Turkish2738 ± 26cP < 0.02.40 ± 8113 ± 19173 ± 1992 ± 16a Data from O'Connor et al. (23O'Connor P.M. Zysow B.R. Schoenhaus S.A. Ishida B.Y. Kunitake S.T. Naya-Vigne J.M. Duchateau P.N. Redberg R.F. Spencer S.J. Mark S. Mazur M. Heilbron D.C. Jaffe R.B. Malloy M.J. Kane J.P. Prebeta-1 HDL in plasma of normolipidemic individuals: influences of plasma lipoproteins, age, and gender.J. Lipid Res. 1998; 39: 670-678Google Scholar).b P < 0.03.c P < 0.02. Open table in a new tab The effect of increasing triglyceride levels on" @default.
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• W2156425270 title "Low levels of high density lipoproteins in Turks, a population with elevated hepatic lipase: high density lipoprotein characterization and gender-specific effects of apolipoprotein E genotype" @default.
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