Obesity is associated with a low-grade
inflammation including moderately increased serum levels of the
acute phase protein serum amyloid A (SAA). In
obesity, SAA is mainly produced from adipose tissue and serum levels of SAA are associated with
insulin resistance. SAA has been described as a
chemoattractant for inflammatory cells and adipose tissue from obese individuals contains increased numbers of macrophages. However, whether adipose tissue-derived SAA can have a direct impact on macrophage infiltration in adipose tissue or the development of
insulin resistance is unknown. The aim of this study was to investigate the effects of adipose tissue-derived SAA1 on the development of
insulin resistance and
obesity-related
inflammation. We have previously established a transgenic mouse model expressing human SAA1 in the adipose tissue. For this report, hSAA1(+/-) transgenic mice and wild type mice were fed with a high fat diet or normal chow. Effects of hSAA1 on
glucose metabolism were assessed using an oral
glucose tolerance test. Real-time PCR was used to measure the
mRNA levels of macrophage markers and genes related to
insulin sensitivity in adipose tissue.
Cytokines during
inflammation were analyzed using a Proinflammatory 7-plex Assay. We found similar
insulin and
glucose levels in hSAA1 mice and wt controls during an oral
glucose tolerance test and no decrease in
mRNA levels of genes related to
insulin sensitivity in adipose tissue in neither male nor female hSAA1 animals. Furthermore, serum levels of proinflammatory
cytokines and
mRNA levels of macrophage markers in adipose tissue were not increased in hSAA1 mice. Hence, in this model we find no evidence that adipose tissue-derived hSAA1 influences the development of
insulin resistance or
obesity-related
inflammation.