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Human Molecular Genetics Advance Access originally published online on April 4, 2006
Human Molecular Genetics 2006 15(10):1650-1658; doi:10.1093/hmg/ddl088
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Genetic linkage of hyperglycemia, body weight and serum amyloid-P in an intercross between C57BL/6 and C3H apolipoprotein E-deficient mice

Zhiguang Su1,2, Yuhua Li1,2, Jessica C. James1,2, Alan H. Matsumoto1, Gregory A. Helm3, Aldons J. Lusis4,5 and Weibin Shi1,2,*

1Department of Radiology, 2Cardiovascular Research Center and 3Department of Neurosurgery, University of Virginia, Charlottesville, VA 22908, USA and 4Department of Medicine and 5Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095-1679, USA

* To whom correspondence should be addressed at: University of Virginia, MR4 Room 1171, PO Box 801339, Charlottesville, VA 22908, USA. Tel: +1 4342439420; Fax: +1 4349825680; Email: ws4v{at}virginia.edu

Received January 3, 2006; Accepted March 30, 2006

Dyslipidemia and hyperglycemia are integral components of the metabolic perturbations in type 2 diabetes. Apolipoprotein E-deficient (apoE–/–) mice develop severe hyperlipidemia and significant hyperglycemia when fed a western diet containing 21% fat (w/w), 0.15% cholesterol and 19.5% casein. Using an intercross between C57BL/6J (B6) and C3H/HeJ (C3H) apoE–/– mice, we performed quantitative trait locus (QTL) analysis to identify loci contributing to hyperglycemia and associated traits. Fasting plasma levels of glucose, insulin and serum amyloid-P (SAP) and body weight in 234 female F2 mice were measured after being fed the western diet for 12 weeks. QTL analysis revealed one significant QTL, named Bglu3 [95.8 cM, logarithm of odds ratio (OR)(LOD) 4.1], on chromosome 1 and a suggestive QTL on chromosome 9 (38 cM, LOD 2.3) that influenced plasma glucose levels. Bglu3 coincided with loci on distal chromosomal 1 that had a major influence on plasma SAP levels and body weight. Significant correlations between plasma glucose, SAP and body weight were observed in F2 mice. Thus, these results demonstrate genetic linkages of hyperglycemia and body weight with SAP, a marker of the acute-phase response, in hyperlipidemic apoE–/– mice and suggest a probability for the Sap gene to be a positional candidate of Bglu3.


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