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1 Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland; Minerva Foundation Institute for Medical Research, Helsinki, Finland
2 Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland
3 Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institutet, Stockholm, Sweden
4 Helsinki University Central Hospital, HUSLAB, Finland
5 Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland; Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institutet, Stockholm, Sweden
* To whom correspondence should be addressed. E-mail: jukka.westerbacka{at}helsinki.fi.
Objective: CCL2 (MCP-1, monocyte chemoattractant protein 1) and CCL3 (MIP-1
, macrophage inflammatory protein 1) are required for macrophage infiltration in adipose tissue. Insulin increases CCL2 expression in adipose tissue and serum more in insulin-resistant obese than in insulin-sensitive lean mice but whether this is true in humans is unknown. Research Methods and Procedures: Subcutaneous adipose tissue biopsies and blood samples were obtained before and at the end of 6 hours of in vivo euglycemic hyperinsulinemia (insulin clamp technique) in 11 lean insulin-sensitive and 10 obese insulin-resistant women, and before and after a 6-hour saline infusion in 8 women. Adipose tissue mRNA concentrations of monocyte/macrophage markers CD68, EMR1, ITGAM, ADAM8, and CCL2 and CCL3, and housekeeping gene RPLP0 were measured using real-time PCR at baseline. Expression of CCL2, CCL3 and RPL0 were measured also after insulin infusion. Serum levels of MCP-1 and MIP- and protein concentration of MCP-1 in adipose tissue were determined at baseline and after insulin infusion. Results: Basally, expression of the macrophage markers CD68 and EMR1 were increased in adipose tissue of insulin-resistant subjects. Insulin increased MCP-1 gene and protein expressionsignificantly more in the insulin-resistant than in the insulin-sensitive subjects. Basally expression of CCL2 and CCL3 and expression of macrophage markers CD68 and ITGAM were significantly correlated. In serum, MCP-1 decreased significantly in insulin-sensitive but not insulin-resistant subjects. MIP-1 was undetectable in serum. Conclusion: Insulin regulation of CCL2 differs between insulin-sensitive and resistant subjects in a direction which could exacerbate adipose tissue inflammation.
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