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Am J Physiol Endocrinol Metab 289: E322-E327, 2005. First published March 15, 2005; doi:10.1152/ajpendo.00408.2004
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apoE4 allele and the natural history of cardiovascular risk factors

Angelo Scuteri,1,2 Samer S. Najjar,1 Denis Muller,3 Reubin Andres,4 Christopher H. Morrell,1,6 Alan B. Zonderman,5 and Edward G. Lakatta1

1Laboratory of Cardiovascular Science, 3Clinical Research Branch, 4Laboratory of Clinical Investigation, and 5Laboratory of Personality and Cognition, National Institute on Aging, National Institutes of Health, Baltimore, Maryland; 2Unità Operativa Geriatria, Istituto Nazionale Ricovero e Cura per Anziani Rome, Italy; and 6Loyola College in Maryland, Baltimore, Maryland

Submitted 8 September 2004 ; accepted in final form 10 March 2005

The aims of the present study were to compare the longitudinal changes in traditional cardiovascular (CV) risk factors (blood pressure, BMI, total and HDL-cholesterol, triglycerides, and blood glucose) in men with and without the apolipoprotein (apo)E4 allele. Three hundred six men from the Baltimore Longitudinal Study of Aging, ranging in age from 20 to 92 yr, were studied. Repeated measurements of CV risk factors were performed over a median follow-up time of 7 yr (maximum 14.3 yr) for men. Longitudinal changes in these CV risk factors were analyzed by linear mixed-effects models. The prevalence of the apoE4 allele was 25.5%. apoE4 was independently associated with accelerated changes over time in fasting plasma glucose (+9.5% vs. no change in those without apoE4 in the 6th age-decade over 10 yr). No significant effect of apoE4 on longitudinal changes in total or HDL-cholesterol, triglycerides, or blood pressures was observed. In conclusion, apoE4 influences fasting plasma glucose and its changes over time. This could explain, in part, the increased CV risk associated with the apoE4 genotype observed in men.

apolipoprotein E4; genetics of vascular disorders; population studies; longitudinal studies; risk factors; glucose



Address for reprint requests and other correspondence: A. Scuteri, Laboratory of Cardiovascular Science, NIA-NIH, 5600 Nathan Shock Dr., Baltimore, MD 21224 (e-mail Scuterian{at}mail.nih.gov)




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