This Article Full Text Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Campos, H. Articles by Ordovás, J. M. Search for Related Content PubMed PubMed Citation Articles by Campos, H. Articles by Ordovás, J. M.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:1074-1081.)
© 1997 American Heart Association, Inc.

Articles

Urbanization Elicits a More Atherogenic Lipoprotein Profile in Carriers of the Apolipoprotein A-IV-2 Allele Than in A-IV-1 Homozygotes

Hannia Campos; José López-Miranda; Carmen Rodríguez; Marta Albajar; Ernst J. Schaefer; ; José M. Ordovás

From the Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (J.L.-M., C.R., M.A., E.J.S., J.M.O.), and the Department of Nutrition, Harvard School of Public Health (H.C.), Boston, Mass.

Correspondence to Hannia Campos, PhD, Department of Nutrition, Room 353A, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115. E-mail hphac{at}gauss.bwh.harvard.edu

Abstract Coronary heart disease (CHD) is increasing in developing countries, particularly in urban areas. The impact of urbanization and apolipoprotein (apo) A-IV genetic polymorphism on plasma lipoproteins was studied in 222 men and 236 women from rural and urban Costa Rica. The apoA-IV allele frequencies were 0.937 for apoA-IV-1 and 0.062 for apoA-IV-2. Significant interactions between the apoA-IV polymorphism and area of residence (rural versus urban) were detected for HDL cholesterol (P=.003), apoA-I (P=.05), LDL particle size (P=.01), and LDL/HDL cholesterol ratio (P=.005). Urban compared with rural carriers of the apoA-IV-2 allele had significantly lower plasma HDL cholesterol (0.95 versus 1.17 mmol/L) and apoA-I (980 versus 1140 mg/L), a significantly higher LDL/HDL cholesterol ratio (3.35 versus 2.39), and significantly smaller LDL particles (258 versus 263 Å). In contrast, no significant rural-urban differences for these parameters were found in apoA-IV-1 homozygotes. Regardless of their apoA-IV phenotype, urban residents consumed more saturated fat (P=.02) and smoked more cigarettes per day (P=.03) than rural residents. A significant interaction between saturated fat intake and apoA-IV phenotype was found for HDL cholesterol (P<.0003) and LDL/HDL cholesterol ratio (P<.003). Increased saturated fat intake (13.6% versus 8.6% of calories) was significantly associated with 6% higher HDL cholesterol and no change (0.7%) in LDL/HDL cholesterol ratio in apoA-IV-1 homozygotes and with 19% lower HDL cholesterol and 37% higher LDL/HDL cholesterol ratio among carriers of the apoA-IV-2 allele. Smokers (1 cigarette per day) had significantly lower HDL cholesterol (P<.005) and apoA-I (P<.01) concentrations than nonsmokers (<1 cigarette per day), particularly among carriers of the apoA-IV-2 allele (-19% and -13%) compared with apoA-IV-1 (-4% for both). After taking these lifestyle characteristics into account, the areas of residence by phenotype interactions for plasma lipoprotein concentrations were no longer statistically significant. Lifestyles associated with an urban environment, such as increased smoking and saturated fat intake, elicit a more adverse plasma lipoprotein profile among Costa Rican carriers of the apoA-IV-2 allele than in apoA-IV-1 homozygotes. Therefore, under the conditions studied, persons with the apoA-IV-2 allele may be more susceptible to CHD.

Key Words: gene polymorphism • LDL particle size • dietary intake • smoking • cholesterol

This article has been cited by other articles:

				H.-h. Chen, B. D. Hosken, M. Huang, J. W. Gaubatz, C. L. Myers, R. D. Macfarlane, H. J. Pownall, and C.-y. Yang Electronegative LDLs from familial hypercholesterolemic patients are physicochemically heterogeneous but uniformly proapoptotic J. Lipid Res., January 1, 2007; 48(1): 177 - 184. [Abstract] [Full Text] [PDF]

				R. Brigelius-Flohe, F. J Kelly, J. T Salonen, J. Neuzil, J.-M. Zingg, and A. Azzi The European perspective on vitamin E: current knowledge and future research Am. J. Clinical Nutrition, October 1, 2002; 76(4): 703 - 716. [Abstract] [Full Text] [PDF]

				R. B. Weinberg, R. A. Anderson, V. R. Cook, F. Emmanuel, P. Denefle, A. R. Tall, and A. Steinmetz Interfacial Exclusion Pressure Determines the Ability of Apolipoprotein A-IV Truncation Mutants to Activate Cholesterol Ester Transfer Protein J. Biol. Chem., June 7, 2002; 277(24): 21549 - 21553. [Abstract] [Full Text] [PDF]

				H. Campos, L. A. Moye, S. P. Glasser, M. J. Stampfer, and F. M. Sacks Low-Density Lipoprotein Size, Pravastatin Treatment, and Coronary Events JAMA, September 26, 2001; 286(12): 1468 - 1474. [Abstract] [Full Text] [PDF]

				S. Q. Ye and P. O Kwiterovich Jr Influence of genetic polymorphisms on responsiveness to dietary fat and cholesterol Am. J. Clinical Nutrition, November 1, 2000; 72 (5): 1275S - 1284S. [Abstract] [Full Text] [PDF]

				R. M. Fisher, H. Burke, V. Nicaud, C. Ehnholm, and S. E. Humphries Effect of variation in the apo A-IV gene on body mass index and fasting and postprandial lipids in the European Atherosclerosis Research Study II J. Lipid Res., February 1, 1999; 40(2): 287 - 294. [Abstract] [Full Text]

				R. Carmena-Ramon, J. F. Ascaso, J. T. Real, J. M. Ordovas, and R. Carmena Genetic Variation at the ApoA-IV Gene Locus and Response to Diet in Familial Hypercholesterolemia Arterioscler Thromb Vasc Biol, August 1, 1998; 18(8): 1266 - 1274. [Abstract] [Full Text] [PDF]