Based on the previously reported observation that monocyte chemoattractant protein-1 (MCP-1) is a key regulator of monocyte infiltration in adipose tissue, Kirk et al. examined whether mice lacking MCP-1 (Mcp1-/-) would have decreased macrophage infiltration and, in turn, increased insulin sensitivity. Surprisingly, independent studies performed at two different facilities at either an early or late time point failed to detect any impairment in macrophage accumulation in adipose tissue in high fat-fed Mcp1-/- mice compared to wild type (WT) mice on the same diet. Knockout mice also had insulin sensitivity indices similar to that of WT mice, with similar plasma levels of glucose, insulin, adiponectin, tumor-necrosis factor-a, and plasminogen activator inhibitor-1. Although MCP-1 was lacking, knockout mice showed higher levels of Mac2, a macrophage-specific protein. These observations led the authors to hypothesize that alternative pathways are probably involved in macrophage recruitment in the inflamed and insulin resistant adipose tissue.
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