Study Title:

Inflammation-Related Immune Cells Cause Excessive New Fat Cells

Study Abstract

Obesity is associated with macrophage infiltration of adipose tissue, which may link adipose inflammation to insulin resistance. However, the impact of inflammatory cells in the pathophysiology of obesity remains unclear. Tartrate resistant acid phosphatase (TRAP) is an enzyme expressed by subsets of macrophages and osteoclasts that exists either as an enzymatically inactive monomer or as an active, proteolytically processed dimer.

Principal Findings
Using mice over expressing TRAP, we show that over-expression of monomeric, but not the dimeric form in adipose tissue leads to early onset spontaneous hyperplastic obesity i.e. many small fat cells. In vitro, recombinant monomeric, but not proteolytically processed TRAP induced proliferation and differentiation of mouse and human adipocyte precursor cells. In humans, monomeric TRAP was highly expressed in the adipose tissue of obese individuals. In both the mouse model and in the obese humans the source of TRAP in adipose tissue was macrophages. In addition, the obese TRAP over expressing mice exhibited signs of a low-grade inflammatory reaction in adipose tissue without evidence of abnormal adipocyte lipolysis, lipogenesis or insulin sensitivity.

Monomeric TRAP, most likely secreted from adipose tissue macrophages, induces hyperplastic obesity with normal adipocyte lipid metabolism and insulin sensitivity.

Study Information

Pernilla Lång, Vanessa van Harmelen, Mikael Rydén, Maria Kaaman, Paolo Parini, Claes Carneheim, A. Ian Cassady, David A. Hume, Göran Andersso, Peter Arner.
Monomeric Tartrate Resistant Acid Phosphatase Induces Insulin Sensitive Obesity
Plos One
2008 March
Karolinska University Hospital, Huddinge, Sweden.

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