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Journal of Lipid Research, Vol. 50, 1353-1362, July 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Serum amyloid A3 does not contribute to circulating SAA levels

Tsuyoshi Chiba^2,*,, Chang Yeop Han^*,, Tomas Vaisar^*,, Kentaro Shimokado, Atil Kargi^*, Mei-Hsiu Chen^*, Shari Wang^*,, Thomas O. McDonald^*, Kevin D. O'Brien^*, Jay W Heinecke^*, and Alan Chait^1,*,

^* Department of Medicine, University of Washington, Seattle, Washington
Diabetes and Obesity Center of Excellence, University of Washington, Seattle, Washington
Department of Vascular Medicine and Geriatrics, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan
² Present address of T. Chiba: Nutritional Science Program, National Institute of Health and Nutrition, 1-23-1, Toyama, Shinjuku-ku, Tokyo, Japan

This work was supported in part by National Institutes of Health Grants HL-030086 and HL-018645; American Heart Association Grant 0830231N; and a Research and Technology Development Award from the Washington Technology Center.

Published, JLR Papers in Press, March 12, 2009.

¹ To whom correspondence should be addressed. e-mail: achait{at}u.washington.edu

Adipose tissue secretes proteins like serum amyloid A (SAA), which plays important roles in local and systemic inflammation. Circulating SAA levels increase in obese humans, but the roles of adipose-derived SAA and hyperlipidemia in this process are unclear. We took advantage of the difference in the inducible isoforms of SAA secreted by adipose tissue (SAA3) and liver (SAA1 and 2) of mice to evaluate whether adipose tissue contributes to the circulating pool of SAA in obesity and hyperlipidemia. Genetically obese (ob/ob) mice, but not hyperlipidemic mice deficient in apolipoprotein E (Apoe^–/–), had significantly higher circulating levels of SAA than their littermate controls. SAA1/2 mRNA expression in the liver and SAA3 mRNA expression in intra-abdominal fat were significantly higher in obese than thin mice, but they were not affected by hyperlipidemia in Apoe^–/– mice. However, only SAA1/2 and the constitutive form of SAA (SAA4) could be detected in the circulation by mass spectrometric analysis of HDL, the major carrier of circulating SAA. In contrast, SAA3 could be detected in medium from cultured adipocytes. Our findings indicate that the expression of SAA3 in adipose tissue is upregulated by obesity, but it does not contribute to the circulating pool of SAA in mice.

Supplementary key words adipose tissue • ApoE deficient mice • gene expression • HDL • local inflammation • ob/ob mice • obesity • systemic inflammation

Abbreviations: Apo, apolipoprotein; CRP, C-reactive protein; FPLC, fast protein liquid chromatography; FPRL1, formyl peptide receptor-like 1; MALDI, matrix-assisted-laser desorption; MCP-1, monocyte chemoattractant protein-1; SAA, serum amyloid A; TNF, tumor necrosis factor; TOF, time of flight

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