A very original investigation on apolipoprotein E-deficient mice was published in the latest issue of Circulation to contribute to the body of evidence suggesting that inflammation associated with intra-abdominal (visceral) adipose tissue accumulation is an important mediator of atherosclerosis. In the study, epididymal (visceral) adipose tissue and subcutaneous fat were transplanted in apo E-/- mice. Even in the absence of marked obesity or diabetes, transplanted intra-abdominal fat was found to be capable of promoting atherosclerosis. This did not occur when subcutaneous fat was transplanted, even though mice in both groups showed a similar degree of macrophage infiltration in adipose tissue. Plasma monocyte chemoattractant protein-1 (MCP-1) levels were also elevated in intra-abdominal fat transplanted mice, and treatment with pioglitazone reduced MCP-1 levels and overall inflammation induced by intra-abdominal adipose tissue. This investigation not only provides a new and useful model to study the inflammatory consequences of intra-abdominal obesity, it also suggests that interventions that target inflammation within intra-abdominal fat may be useful in reducing the vascular risk associated with this harmful adipose depot.
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