Serum amyloid A3 does not contribute to circulating SAA levels

Tsuyoshi Chiba, Chang Yeop Han, Tomas Valsar, Kentaro Shimokado, Atil Kargi, Mei Hsiu Chen, Shari Wang, Thomas O. McDonald, Kevin D. O'Brien, Jay W. Heinecke, Alan Chait

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1353-1362
Number of pages10
JournalJournal of Lipid Research
Volume50
Issue number7
DOIs
StatePublished - Jul 1 2009
Externally publishedYes

Fingerprint

Serum Amyloid A Protein
Amyloid
Serum
Adipose Tissue
Hyperlipidemias
Tissue
Apolipoproteins E
Liver
Obesity
Obese Mice
Messenger RNA
Intra-Abdominal Fat
Adipocytes
Protein Isoforms
Fats
Inflammation

Keywords

  • Adipose tissue
  • ApoE deficient mice
  • Gene expression
  • HDL
  • Local inflammation
  • Ob/ob mice
  • Obesity
  • Systemic inflammation

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Endocrinology

Cite this

Chiba, T., Han, C. Y., Valsar, T., Shimokado, K., Kargi, A., Chen, M. H., ... Chait, A. (2009). Serum amyloid A3 does not contribute to circulating SAA levels. Journal of Lipid Research, 50(7), 1353-1362. https://doi.org/10.1194/jlr.M900089-JLR200

Serum amyloid A3 does not contribute to circulating SAA levels. / Chiba, Tsuyoshi; Han, Chang Yeop; Valsar, Tomas; Shimokado, Kentaro; Kargi, Atil; Chen, Mei Hsiu; Wang, Shari; McDonald, Thomas O.; O'Brien, Kevin D.; Heinecke, Jay W.; Chait, Alan.

In: Journal of Lipid Research, Vol. 50, No. 7, 01.07.2009, p. 1353-1362.

Research output: Contribution to journalArticle

Chiba, T, Han, CY, Valsar, T, Shimokado, K, Kargi, A, Chen, MH, Wang, S, McDonald, TO, O'Brien, KD, Heinecke, JW & Chait, A 2009, 'Serum amyloid A3 does not contribute to circulating SAA levels', Journal of Lipid Research, vol. 50, no. 7, pp. 1353-1362. https://doi.org/10.1194/jlr.M900089-JLR200
Chiba, Tsuyoshi ; Han, Chang Yeop ; Valsar, Tomas ; Shimokado, Kentaro ; Kargi, Atil ; Chen, Mei Hsiu ; Wang, Shari ; McDonald, Thomas O. ; O'Brien, Kevin D. ; Heinecke, Jay W. ; Chait, Alan. / Serum amyloid A3 does not contribute to circulating SAA levels. In: Journal of Lipid Research. 2009 ; Vol. 50, No. 7. pp. 1353-1362.
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