The metabolic syndrome: A crossroad for genotype-phenotype associations in atherosclerosis

被引：24

作者：

Corella D. ^{[1
]}

Ordovas J.M. ^{[1
]}

机构：

[1] Nutrition and Genomics Laboratory, Department of Agriculture, Tufts University, Boston, MA 02111

来源：

Current Atherosclerosis Reports | 2004年 / 6卷 / 3期

基金：

美国国家卫生研究院;

关键词：

Metabolic Syndrome; Cholesteryl Ester Transfer Protein; Arterioscler Thromb Vasc Biol; Hepatic Lipase; Microsomal Triglyceride Transfer Protein;

D O I：

10.1007/s11883-004-0031-8

中图分类号：

学科分类号：

摘要：

The metabolic syndrome comprises a set of metabolic and physiologic risk factors associated with elevated cardiovascular disease risk. The expression of each one of its major factors (hypertriglyceridemia, low high-density lipoprotein cholesterol levels, hypertension, abdominal obesity, and insulin resistance) has been found to be the result of complex interactions between genetic and environmental factors. Moreover, obesity may play a major role in triggering the metabolic syndrome by interacting with genetic variants at candidate genes for dyslipidemia, hypertension, and insulin resistance. In support of this hypothesis, several studies at multiple candidate genes have already demonstrated the significance of these interactions; however, the data and their reliability are still very limited, and in many cases replication studies are still lacking in the literature. Therefore, more studies with better epidemiologic design and standardized adiposity measures are needed to estimate the contribution of body weight and fat distribution to the genetic predisposition to the metabolic syndrome, which is the most common cardiovascular disease risk factor in industrialized societies. Copyright © 2004 by Current Science Inc.

引用

页码：186 / 196

页数：10

共 67 条

[51]

Strazzullo P., Jacone R., Iacoviello L., Et al., Genetic variation in the renin-angiotensin system and abdominal adiposity in men: The Olivetti Prospective Heart Study, Ann. Intern. Med., 138, pp. 17-23, (2003)

[52]

Tabara Y., Kohara K., Nakura J., Miki T., Risk factor-gene interaction in carotid atherosclerosis: Effect of gene polymorphisms of renin-angiotensin system, J. Hum. Genet., 46, pp. 278-284, (2001)

[53]

Elosua R., Demissie S., Cupples L.A., Et al., Obesity modulates the association among apoe genotype, insulin, and glucose in men, Obes. Res., 11, pp. 1502-1508, (2003)

[54]

Ukkola O., Rankinen T., Weisnagel S.J., Et al., Interactions among the alpha2-, beta2-, and beta3-adrenergic receptor genes and obesity-related phenotypes in the Quebec Family Study, Metabolism, 49, pp. 1063-1070, (2000)

[55]

Elbein S.C., Chu W., Ren Q., Et al., Role of calpain-10 gene variants in familial type 2 diabetes in Caucasians, J. Clin. Endocrinol. Metab., 87, pp. 650-654, (2002)

[56]

Hsu L.A., Ko Y.L., Hsu K.H., Et al., Genetic variations in the cholesteryl ester transfer protein gene and high density lipoprotein cholesterol levels in Taiwanese Chinese, Hum. Genet., 110, pp. 57-63, (2002)

[57]

Freeman D.J., Griffin B.A., Holmes A.P., Et al., 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., 14, pp. 336-344, (1994)

[58]

Heilbronn L.K., Noakes M., Clifton P.M., Association between HDL-cholesterol and the Taq1B polymorphism in the cholesterol ester transfer protein gene in obese women, Atherosclerosis, 162, pp. 419-424, (2002)

[59]

Vohl M.C., Lamarche B., Pascot A., Et al., Contribution of the cholesteryl ester transfer protein gene TaqIB polymorphism to the reduced plasma HDL-cholesterol levels found in abdominal obese men with the features of the insulin resistance syndrome, Int. J. Obes. Relat. Metab. Disord., 23, pp. 918-925, (1999)

[60]

Garenc C., Perusse L., Chagnon Y.C., Et al., The hormone-sensitive lipase gene and body composition: The HERITAGE Family Study, Int. J. Obes. Relat. Metab. Disord., 26, pp. 220-227, (2002)

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