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• W2114804938 abstract "HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 20, No. 8Lipids, Lipases, and Obesity Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBLipids, Lipases, and Obesity Does Race Matter? Peter W. F. Wilson Peter W. F. WilsonPeter W. F. Wilson From the Framingham Heart Study, Boston University School of Medicine, Framingham, Mass. Search for more papers by this author Originally published1 Aug 2000https://doi.org/10.1161/01.ATV.20.8.1854Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1854–1856For >20 years, researchers have reported that American blacks tend to have lower triglyceride and higher HDL cholesterol (HDL-C) levels compared with whites at a similar level of corpulence.12 Early studies focused on potential environmental explanations and concluded that differences in exercise, alcohol intake, leanness, and undernutrition did not readily account for the higher HDL-C levels.3 It was also noted that the propensity toward more favorable HDL-C and triglyceride levels was absent in highly educated blacks.4 More recent reports have shown that socioeconomic status was positively correlated with HDL-C in white men and women, a negative association was present in black men, and no association was evident in black women.5Autopsy reports have also demonstrated differences in atherosclerosis in blacks versus whites. The Bogalusa Study6 reported that young blacks had more fatty streaks than did whites but that middle-aged blacks had less evidence of fibrous plaques. The authors concluded that the transition of fatty streaks to advanced atherosclerotic lesions may differ in whites and blacks.6 Similar results were obtained in the Pathobiological Determinants of Atherosclerosis in Youth study,7 an autopsy investigation of young adults who died from trauma between the ages of 15 to 34 years. Adolescent blacks in that study had a greater extent of fatty streaks than did whites, but older blacks and whites had a similar extent of raised lesions.7The associations of sex, race, obesity, and fat metabolism have been under intense study as coronary heart disease mortality has declined, but Americans have ballooned in size over the past 2 decades. The article in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology by Després et al8 highlights metabolic differences in a systematic comparison of lipids, obesity, and lipase activity in a well-designed multicenter North American study that included blacks and whites.Després et al8 demonstrate effectively that blacks are less likely than whites to be viscerally obese. In addition, plasma hepatic lipase activity is less and lipoprotein lipase activity is greater in blacks after intravenous heparin infusion. These results suggest indirectly that a fat load can be cleared more efficiently by blacks than by whites. The findings are muted by multivariate regression analysis, but the primary result is unassailable: lipolytic activity is greater and visceral obesity is less in the black participants.Cardiovascular risk factor reports in obese individuals have recently demonstrated a remarkable number of metabolic abnormalities that embrace differences in lipids, glycemia, insulin, blood pressure, and hematologic function.91011 We now have several names for syndromes that are similar and include the clustering of metabolic risk factors. In fact, Sniderman et al12 have suggested that hyperapolipoproteinemia B, familial combined hyperlipidemia, syndrome X, the plurimetabolic syndrome, the visceral fat syndrome, familial dyslipidemic hypertension, the atherogenic lipoprotein phenotype, and the deadly quartet share a common pathophysiology.There is a need for improved metabolic profiling of obese persons that participate in larger surveys. We already have dynamic testing for glycemic responses to oral and intravenous glucose loads, and a variety of techniques are available to assess glucose and insulin response.1314 Population research suggests that a 2-hour oral glucose tolerance is adequate for many studies, and fasting insulin is key in the study of insulin resistance.15Fat-load studies are a traditional way to characterize fat metabolism, but protocols are somewhat cumbersome and typically take at least 4 hours after the initial fat load.16 Fat-loading data suggest differences between whites and blacks. For instance, carotid intimal medial thickness was positively associated with postprandial responses of triglycerides and triglyceride-rich lipoproteins in white men and women but not in blacks in the Atherosclerosis Risk in Communities study.16 These results were obtained only in persons with a body mass index <30 kg/m2. The postprandial lipid associations were not statistically significant after adjustment for fasting lipids, and the authors concluded that postprandial triglycerides must be accompanied by the accumulation of triglyceride-rich lipoprotein remnants to be atherogenic.16 A recent fat clearance study in young adults found that blacks cleared a fat load more efficiently than did whites. In that investigation, postprandial triglycerides were negatively correlated with lipoprotein lipase in blacks and whites, whereas postprandial triglyceride response was positively correlated with hepatic lipase activity in whites and negatively correlated in blacks.Newer assays can determine the densities for a spectrum of lipid particles by nuclear magnetic resonance testing or gradient gel electrophoresis.1718 These techniques have the promise to be helpful in characterizing population groups.1920 Also available are assays of triglyceride-rich lipid remnants, which can be measured in the fasting state. Preliminary studies suggest that higher levels of triglyceride-rich remnant particles are positively associated with a greater prevalence of coronary disease.2021Després et al8 used postheparin lipase profiling in their study and compared hepatic lipase and lipoprotein lipase activities after a heparin infusion. Because the study highlights differences in visceral obesity and lipase activity that appear to be based on ethnicity, it is natural to consider the importance of the genetic underpinnings for such findings. Are blacks more likely to have specific genetic variations in lipases that might help to explain the lipid and visceral tendencies? Several polymorphisms are under study, and research is focusing on the cholesteryl ester transfer protein, apolipoprotein AI/CIII/AIV, and hepatic lipase loci.222324A polymorphism within the hepatic lipase promoter (−514C→T), which is present in ≈36% of middle-aged Framingham Heart Study participants, has been relatively consistently associated with higher HDL-C,25 and it has been suggested the HDL2 fraction is particularly increased.2627 In addition, Vega et al28 have reported that the −514T hepatic lipase allele is more common in blacks than in whites. This genetic variant, and potentially others, may help to explain the relative advantage that blacks have for higher HDL-C, although this polymorphism may not be key to the effects. Linkage disequilibrium with another gene or another polymorphism may be responsible for the phenotypic expression.Although coronary mortality has declined over the past 3 decades, our society is still unsettled by a large burden of coronary artery disease and stroke. There have been declines in blood pressure, cholesterol, and cigarette smoking, but as we have rallied forces to battle these risk factors, we have been outflanked by the adipocyte. Recently published National Health and Nutrition Examination Survey III data,29 undertaken between 1988 to 1994, demonstrate obesity (>30 kg/m2) in ≈22% of white and black men and in ≈24% and 38% of white and black women, respectively. These national survey data, taken with the results from the report of Després et al,8 suggest that environmental factors may be removing any natural advantage that blacks may have toward more favorable lipid profiles. Efforts to control lipid levels and vascular disease risk in blacks and whites need to consider the current obesity epidemic, recognizing that the age-adjusted prevalence of obesity in the United States is still on the rise.Dr Wilson is partially supported by a grant from Roche Laboratories.FootnotesCorrespondence to Peter W.F. Wilson, MD, Framingham Heart Study, Boston University School of Medicine, 5 Thurber St, Framingham, MA 01702. E-mail [email protected] References 1 Morrison JA, Khoury P, Mellies M, Kelly K, Horvitz R, Glueck CJ. Lipid and lipoprotein distributions in black adults: the Cincinnati Lipid Research Clinic’s Princeton School Study. JAMA.1981; 245:939–942.CrossrefMedlineGoogle Scholar2 Morrison JA, deGroot I, Kelly KA, Mellies MJ, Khoury P, Edwards BK, Lewis D, Lewis A, Fiorelli M, Heiss G, et al. Black-white differences in plasma lipids an lipoproteins in adults: the Cincinnati Lipid Research Clinic Population Study. Prev Med.1979; 8:34–39.CrossrefMedlineGoogle Scholar3 Gartside PS, Khoury P, Glueck CJ. Determinants of high-density lipoprotein cholesterol in blacks and whites: the second National Health and Nutrition Examination Survey. Am Heart J.1984; 108:641–653.CrossrefMedlineGoogle Scholar4 Wilson PW, Savage DD, Castelli WP, Garrison RJ, Donahue RP, Feinleib M. HDL-cholesterol in a sample of black adults: the Framingham Minority Study. Metabolism.1983; 32:328–332.CrossrefMedlineGoogle Scholar5 Metcalf PA, Sharrett AR, Folsom AR, Duncan BB, Patsch W, Hutchinson RG, Szklo M, Davis CE, Tyroler HA. African American-white differences in lipids, lipoproteins, and apolipoproteins, by educational attainment, among middle-aged adults: the Atherosclerosis Risk in Communities Study. Am J Epidemiol.1998; 148:750–760.CrossrefMedlineGoogle Scholar6 Freedman DS, Newman WP, Tracy RE, Voors AE, Srinivasan SR, Webber LS, Restrepo C, Strong JP, Berenson GS. Black-white differences in aortic fatty streaks in adolescence and early adulthood: the Bogalusa Heart Study. Circulation..1988; 77:856–864.CrossrefMedlineGoogle Scholar7 McGill HCJ, McMahan CA, Malcom GT, Oalmann MC, Strong JP. Effects of serum lipoproteins and smoking on atherosclerosis in young men and women: the PDAY Research Group: Pathobiological Determinants of Atherosclerosis in Youth. Arterioscler Thromb Vasc Biol.1997; 17:95–106.CrossrefMedlineGoogle Scholar8 Després JP, Couillard C, Gagnon J, Bergeron N, Leon AS, Rao DC, Skinner JS, Wilmore JH, Bouchard C. Race, visceral adipose tissue, plasma lipids, and lipoprotein lipase activity in men and women: the health, risk factors, exercise training, and genetics (HERITAGE) family study. Arterioscler Thromb Vasc Biol..2000; 20:1932–1938.CrossrefMedlineGoogle Scholar9 Meigs JB, D’Agostino RB, Wilson PWF, Cupples LA, Nathan DM, Singer DE. Risk variable clustering in the insulin resistance syndrome. Diabetes.1997; 46:1594–1600.CrossrefMedlineGoogle Scholar10 Meigs JB, Mittleman MA, Nathan DM, Tofler GH, Singer DE, Murphy-Sheehy PM, Lipinska I, D’Agostino RB, Wilson PWF. Hyperinsulinemia, hyperglycemia, and impaired hemostasis: the Framingham Offspring Study. JAMA..2000; 283:221–228.CrossrefMedlineGoogle Scholar11 Reaven GM. Banting Lecture 1988: role of insulin resistance in human disease. Diabetes.1988; 37:1595–1607.CrossrefMedlineGoogle Scholar12 Sniderman AD, Pedersen T, Kjekshus J. Putting low-density lipoproteins at center stage in atherogenesis. Am J Cardiol.1997; 79:64–67.CrossrefMedlineGoogle Scholar13 Reaven GM. Pathophysiology of insulin resistance in human disease. Physiol Rev.1995; 75:473–486.CrossrefMedlineGoogle Scholar14 Reaven GM, Laws A. Insulin resistance, compensatory hyperinsulinaemia, and coronary heart disease. Diabetologia.1994; 37:948–952.CrossrefMedlineGoogle Scholar15 Laakso M. How good a marker is insulin level for insulin resistance? Am J Epidemiol..1993; 137:959–965.CrossrefMedlineGoogle Scholar16 Sharrett AR, Chambless LE, Heiss G, Paton CC, Patsch W. Association of postprandial triglyceride and retinyl palmitate responses with asymptomatic carotid artery atherosclerosis in middle-aged men and women: the Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb Vasc Biol.1995; 15:2122–2129.CrossrefMedlineGoogle Scholar17 Otvos JD. Measurement of lipoprotein subclass profiles by nuclear magnetic resonance spectroscopy. In: Rifai N, Warnick GR, Dominiczak MH, ed. Handbook of Lipoprotein Testing. Washington, DC: AACC Press; 1997:497–508.Google Scholar18 Krauss RM. Relationship of intermediate and low density lipoprotein subspecies to risk of coronary artery disease. Am Heart J.1987; 113:578–581.CrossrefMedlineGoogle Scholar19 Nakajima K, Saito T, Tamura A, Suzuki M, Nakano T, Adachi M, Tanaka A, Tada N, Nakamura H, Campos E. Cholesterol in remnant-like lipoproteins in human serum using monoclonal anti apo B-100 and anti apo A-I immunoaffinity mixed gels. Clin Chim Acta.1993; 223:53–71.CrossrefMedlineGoogle Scholar20 McNamara JR, Shah PK, Nakajima K, Cupples LA, Wilson PW, Ordovas JM, Schaefer EJ. Remnant lipoprotein cholesterol and triglyceride reference ranges from the Framingham Heart Study. Clin Chem. 1998;44(pt 1):1224–1232.Google Scholar21 Ordovas JM, Cupples LA, Wilson PWF, Lahoz C, Levy D, Otvos J, McNamara JR, Gagne C, Hayden M SE. Advances in cardiovascular risk prediction: new biochemical and genetic markers. In: Jacotot B, Mathe D, Fruchart J-C, ed. Atherosclerosis XI. Amsterdam, the Netherlands: Elsevier; 1998:425–434.Google Scholar22 Guerra R, Wang J, Grundy SM, Cohen JC. A hepatic lipase (LIPC) allele associated with high plasma concentrations of high density lipoprotein cholesterol. Proc Natl Acad Sci U S A.1997; 94:4532–4537.CrossrefMedlineGoogle Scholar23 Cohen JC, Wang Z, Grundy SM, Stoesz MR, 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; 94:2377–2384.CrossrefMedlineGoogle Scholar24 Freeman DJ, Griffin BA, Holmes AP, Lindsay GM, Gaffney D, Packard CJ, Shepherd J. Regulation of plasma HDL cholesterol and subfraction distribution by genetic and environmental factors: associations between the TaqI B RFLP in the CETP gene and smoking and obesity. Arterioscler Thromb.1994; 14:336–344.CrossrefMedlineGoogle Scholar25 Allayee H, Dominguez KM, Aouizerat BE, Krauss RM, Rotter JI, Lu J, Cantor RM, de Bruin TW, Lusis AJ. Contribution of the hepatic lipase gene to the atherogenic lipoprotein phenotype in familial combined hyperlipidemia. J Lipid Res..2000; 41:245–252.CrossrefMedlineGoogle Scholar26 Couture P, Otvos JD, Cupples LA, Lahoz C, Wilson PW, Schaefer EJ, Ordovas JM. Association of the C-514T polymorphism in the hepatic lipase gene with variations in lipoprotein subclass profiles: the Framingham Offspring Study. Arterioscler Thromb Vasc Biol..2000; 20:815–822.CrossrefMedlineGoogle Scholar27 Grundy SM, Vega GL, Otvos JD, Rainwater DL, Cohen JC. Hepatic lipase activity influences high density lipoprotein subclass distribution in normotriglyceridemic men: genetic and pharmacological evidence. J Lipid Res.1999; 40:229–234.CrossrefMedlineGoogle Scholar28 Vega GL, Clark LT, Tang A, Marcovina S, Grundy SM, Cohen JC. Hepatic lipase activity is lower in African American men than in white American men: effects of 5′ flanking polymorphism in the hepatic lipase gene (LIPC). J Lipid Res.1998; 39:228–232.CrossrefMedlineGoogle Scholar29 Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. JAMA.1999; 282:1523–1529.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Shah D, Grimes C, Brown E and Hwang L (2011) Demographics, socio-behavioral factors, and drug use patterns: What matters in spontaneous HCV clearance?, Journal of Medical Virology, 10.1002/jmv.22271, 84:2, (235-241), Online publication date: 1-Feb-2012. Iliadou A, Snieder H, Wang X, Treiber F and Davis C (2012) Heritabilities of Lipids in Young European American and African American Twins, Twin Research and Human Genetics, 10.1375/twin.8.5.492, 8:5, (492-498), Online publication date: 1-Oct-2005. Samman S (2001) Nutrition and metabolism, Current Opinion in Lipidology, 10.1097/00041433-200104000-00014, 12:2, (221-222), Online publication date: 1-Apr-2001. Jakubowski H, Ambrosius W and Pratt J (2001) Genetic determinants of homocysteine thiolactonase activity in humans: implications for atherosclerosis, FEBS Letters, 10.1016/S0014-5793(01)02143-3, 491:1-2, (35-39), Online publication date: 23-Feb-2001. August 2000Vol 20, Issue 8 Advertisement Article InformationMetrics https://doi.org/10.1161/01.ATV.20.8.1854 Originally publishedAugust 1, 2000 KeywordsobesityEditorialslipaseslipidsPDF download Advertisement" @default.
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