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Establishment of a transgenic mouse model specifically expressing human serum amyloid a in adipose tissue.

Artikel i vetenskaplig tidskrift
Författare Maja Olsson
Sofie Ahlin
Bob Olsson
Per-Arne Svensson
Marcus Ståhlman
Jan Borén
Lena M S Carlsson
Kajsa Sjöholm
Publicerad i PloS one
Volym 6
Nummer/häfte 5
Sidor e19609
ISSN 1932-6203
Publiceringsår 2011
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor e19609
Språk en
Länkar dx.doi.org/10.1371/journal.pone.001...
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Obesity and obesity co-morbidities are associated with a low grade inflammation and elevated serum levels of acute phase proteins, including serum amyloid A (SAA). In the non-acute phase in humans, adipocytes are major producers of SAA but the function of adipocyte-derived SAA is unknown. To clarify the role of adipocyte-derived SAA, a transgenic mouse model expressing human SAA1 (hSAA) in adipocytes was established. hSAA expression was analysed using real-time PCR analysis. Male animals were challenged with a high fat (HF) diet. Plasma samples were subjected to fast protein liquid chromatography (FPLC) separation. hSAA, cholesterol and triglyceride content were measured in plasma and in FPLC fractions. Real-time PCR analysis confirmed an adipose tissue-specific hSAA gene expression. Moreover, the hSAA gene expression was not influenced by HF diet. However, hSAA plasma levels in HF fed animals (37.7±4.0 µg/mL, n = 7) were increased compared to those in normal chow fed animals (4.8±0.5 µg/mL, n = 10; p<0.001), and plasma levels in the two groups were in the same ranges as in obese and lean human subjects, respectively. In FPLC separated plasma samples, the concentration of hSAA peaked in high-density lipoprotein (HDL) containing fractions. In addition, cholesterol distribution over the different lipoprotein subfractions as assessed by FPLC analysis was similar within the two experimental groups. The established transgenic mouse model demonstrates that adipose tissue produced hSAA enters the circulation, resulting in elevated plasma levels of hSAA. This new model will enable further studies of metabolic effects of adipose tissue-derived SAA.

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