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Age-Accelerated Atherosclerosis Correlates With Failure to Upregulate Antioxidant Genes

Age-Accelerated Atherosclerosis Correlates With Failure to Upregulate Antioxidant Genes UltraRapid Communication Age-Accelerated Atherosclerosis Correlates With Failure to Upregulate Antioxidant Genes Alan R. Collins, Christopher J. Lyon, Xuefeng Xia, Joey Z. Liu, Rajendra K. Tangirala, Fen Yin, Rima Boyadjian, Alfiya Bikineyeva, Domenico Pratico`, David G. Harrison, Willa A. Hsueh Abstract—Excess food intake leads to obesity and diabetes, both of which are well-known independent risk factors for atherosclerosis, and both of which are growing epidemics in an aging population. We hypothesized that aging enhances the metabolic and vascular effects of high fat diet (HFD) and therefore examined the effect of age on atherosclerosis and insulin resistance in lipoprotein receptor knockout (LDLR ) mice. We found that 12-month-old (middle-aged) LDLR mice developed substantially worse metabolic syndrome, diabetes, and atherosclerosis than 3-month-old (young) LDLR mice when both were fed HFD for 3 months, despite similar elevations in total cholesterol levels. Microarray analyses were performed to analyze the mechanism responsible for the marked acceleration of atheroscle- rosis in middle-aged mice. Chow-fed middle-aged mice had greater aortic expression of multiple antioxidant genes than chow-fed young mice, including glutathione peroxidase-1 and -4, catalase, superoxide dismutase-2, and uncoupling protein-2. Aortic expression of these enzymes markedly increased in young mice fed HFD but decreased or only modestly http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation Research Wolters Kluwer Health

Age-Accelerated Atherosclerosis Correlates With Failure to Upregulate Antioxidant Genes

Hsueh, Willa A.
Circulation Research , Volume 104 (6) – Mar 1, 2009
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ISSN
0009-7330
eISSN
1524-4571
DOI
10.1161/CIRCRESAHA.108.188771
pmid
19265038
Publisher site
See Article on Publisher Site

Abstract

UltraRapid Communication Age-Accelerated Atherosclerosis Correlates With Failure to Upregulate Antioxidant Genes Alan R. Collins, Christopher J. Lyon, Xuefeng Xia, Joey Z. Liu, Rajendra K. Tangirala, Fen Yin, Rima Boyadjian, Alfiya Bikineyeva, Domenico Pratico`, David G. Harrison, Willa A. Hsueh Abstract—Excess food intake leads to obesity and diabetes, both of which are well-known independent risk factors for atherosclerosis, and both of which are growing epidemics in an aging population. We hypothesized that aging enhances the metabolic and vascular effects of high fat diet (HFD) and therefore examined the effect of age on atherosclerosis and insulin resistance in lipoprotein receptor knockout (LDLR ) mice. We found that 12-month-old (middle-aged) LDLR mice developed substantially worse metabolic syndrome, diabetes, and atherosclerosis than 3-month-old (young) LDLR mice when both were fed HFD for 3 months, despite similar elevations in total cholesterol levels. Microarray analyses were performed to analyze the mechanism responsible for the marked acceleration of atheroscle- rosis in middle-aged mice. Chow-fed middle-aged mice had greater aortic expression of multiple antioxidant genes than chow-fed young mice, including glutathione peroxidase-1 and -4, catalase, superoxide dismutase-2, and uncoupling protein-2. Aortic expression of these enzymes markedly increased in young mice fed HFD but decreased or only modestly

Journal

Circulation Research – Wolters Kluwer Health

Published: Mar 1, 2009

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