Published online before print September 15, 2005, doi: 10.1161/01.ATV.0000186365.73973.f0
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© 2005 American Heart Association, Inc.
Brief Reviews |
Dietary and Genetic Probes of Atherogenic Dyslipidemia
From Children’s Hospital Oakland Research Institute, Oakland, Calif.
Correspondence to Ronald M. Krauss, MD, Children’s Hospital Oakland Research Institute, 5700 Martin Luther King, Jr Way, Oakland, CA 94609. E-mail RKrauss{at}chori.org
A goal of dietary management of cardiovascular disease risk in patients with obesity and metabolic syndrome is improvement in the atherogenic dyslipidemia comprising elevated triglyceride, reduced high-density lipoprotein (HDL) cholesterol, and increased numbers of small, dense low-density lipoprotein (LDL) particles. Individuals with a genetically influenced trait characterized by a high proportion of small, dense LDL (phenotype B) respond to a low-fat, high-carbohydrate diet with greater reduction of LDL cholesterol, apoprotein B, and mid-sized LDL2 particles than unaffected subjects (phenotype A). In contrast, in phenotype A subjects there is a reciprocal shift from large LDL1 to small LDL3 such that a high proportion convert to phenotype B. There is evidence for heritable effects on these diet-induced subclass changes and for the involvement of specific genes. For example, a haplotype of the APOA5 gene associated with increased plasma triglyceride and small, dense LDL predicts greater diet-induced reduction of LDL2, a haplotype-specific effect that is strongly correlated with both increased VLDL precursors and LDL4 products. Understanding of such diet-genotype interactions may help to elucidate mechanisms that are responsible for phenotype B and for its differential dietary responsiveness. This information may also ultimately help in identifying those individuals who are most likely to achieve cardiovascular risk benefit from specific dietary interventions.
Dietary and genetic factors can interact to generate a phenotype characterized by an increase in small dense LDL particles that is a component of the atherogenic dyslipidemia of the metabolic syndrome. Genotypes associated with responses of lipoprotein subspecies to changes in dietary carbohydrate and fat can contribute to interindividual variability in LDL response to diet.
Key Words: lipoproteins • diet • genetics • genetic polymorphisms
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