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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #90310
Title: URBANIZATION ELICITS A MORE ATHEROGENIC LIPOPROTEIN PROFILE IN CARRIERS OF THE APOLIPOPROTEIN A-IV-2 ALLELE THAN IN A-IV-1 HOMOZYGOTES

Author
item CAMPOS, HANNIA - HARVARD SCH PUBL HEALTH
item LOPEZ-MIRANDA, JOSE - HNRCA-TUFTS
item RODRIGUEZ, CARMEN - HNRCA-TUFTS
item ALBAJAR, MARTA - HNRCA-TUFTS
item SCHAEFER, ERNST - HNRCA-TUFTS
item ORDOVAS, JOSE - HNRCA-TUFTS

Submitted to: Arteriosclerosis Thrombosis and Vascular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/2/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Coronary heart disease (CHD) is increasing in developing countries, particularly in urban areas. Genetic factors and their interaction with the environment may play an important role in these effects. We have studied the possible association between a genetic mutation in apolipoprotein A-IV (an important component of intestinal lipoproteins) on blood cholesterol levels using two groups of subjects in Costa Rica subjected to different life styles: urban and rural. Our data demonstrates that mutations at the apolipoprotein A-IV gene exerts different effects depending on the diet and other habits of these indivuduals. In summary, lifestyles associated with an urban environment, such as increased smoking and saturated fat intake, elicit a more adverse blood cholesterol profile among Costa Rican carriers of the apoA-IV mutation than in non-carriers. Therefore, under the conditions studied, persons with the apoA-IV mutation may be more susceptible to CHD.

Technical Abstract: 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. 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 A). Urban residents consumed more saturated fat and smoked more cigarettes per day than rural residents. A significant interaction between saturated fat intake and apoA-IV phenotype was found for HDL cholesterol and LDL/HDL cholesterol ratio. Increased saturated fat intake was significantly associated with 6% higher HDL cholesterol and no change 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 had significantly lower HDL cholesterol and apoA-I concentrations than nonsmokers, particularly among carriers of the apoA-IV-2 allele compared with apoA-IV-1. 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.