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Am J Physiol Endocrinol Metab 294: E841-E845, 2008. First published February 12, 2008; doi:10.1152/ajpendo.00653.2006
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Insulin regulation of MCP-1 in human adipose tissue of obese and lean women

Jukka Westerbacka,1,2 Anja Cornér,1 Maria Kolak,3 Janne Makkonen,1,2 Ursula Turpeinen,4 Anders Hamsten,3 Rachel M. Fisher,3 and Hannele Yki-Järvinen1,2

1University of Helsinki, Department of Medicine, Division of Diabetes, and 2Minerva Medical Research Institute, Helsinki, Finland; 3Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institutet, Stockholm, Sweden; 4HUSLAB, Helsinki University Central Hospital, Helsinki, Finland

Submitted 30 November 2006 ; accepted in final form 27 December 2007

CCL2 (MCP-1, monocyte chemoattractant protein 1) and CCL3 (MIP-1{alpha}, macrophage inflammatory protein 1{alpha}) are required for macrophage infiltration in adipose tissue. Insulin increases CCL2 expression in adipose tissue and in serum more in insulin-resistant obese than in insulin-sensitive lean mice, but whether this is true in humans is unknown. We compared basal expression and insulin regulation of CCL2 and CCL3 in adipose tissue and MCP-1 and MIP-1{alpha} in serum between insulin-resistant and insulin-sensitive human subjects. Subcutaneous adipose tissue biopsies and blood samples were obtained before and at the end of 6 h of in vivo euglycemic hyperinsulinemia (maintained by the insulin clamp technique) in 11 lean insulin-sensitive and 10 obese insulin-resistant women, and before and after a 6-h saline infusion in 8 women. Adipose tissue mRNA concentrations of monocyte/macrophage markers CD68, EMR1, ITGAM, ADAM8, chemokines CCL2 and CCL3, and housekeeping gene ribosomal protein large P0 (RPLP0) were measured by means of real-time PCR at baseline. In addition, mRNA concentrations of CCL2, CCL3, and RPLP0 were measured after insulin infusion. Levels of MCP-1 and MIP-1{alpha} were determined in serum, and protein concentration of MCP-1 was determined in adipose tissue at baseline and after insulin infusion. 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 expression significantly 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{alpha} was undetectable in serum. Insulin regulation of CCL2 differs between insulin-sensitive and -resistant subjects in a direction that could exacerbate adipose tissue inflammation.

adipocytes; adipokines; insulin sensitivity; monocyte chemoattractant protein


Address for reprint requests and other correspondence: Jukka Westerbacka, Dept. of Medicine, Division of Diabetes, Univ. of Helsinki, P.O. Box 700, Rm. C418b, Biomedicum, FIN-00029 HUCH, Helsinki, Finland (e-mail: jukka.westerbacka{at}helsinki.fi)




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