Obesity is accompanied by the presence of chronic low grade inflammation manifested by infiltration of macrophages into adipose tissue. Mannose-binding lectin (MBL), a soluble mediator of innate immunity, promotes phagocytosis and alters macrophage function. To assess the function of MBL in the development of obesity, we studied WT and MBL-/- mice rendered obese by high fat feeding (HFD). Whereas no gross morphological differences were observed in liver, HFD feeding provoked distinct changes in adipose tissue morphology of MBL-/- mice. In parallel with increased adipocyte size, MBL-/- mice displayed increased influx of macrophages into adipose tissue. Macrophages were polarized towards an alternatively activated phenotype known to modulate apoptotic cell clearance. MBL deficiency also significantly increased the number of apoptotic cells in adipose tissue. Consistent with these observations, recombinant MBL enhanced phagocytic capacity of the stromal vascular fraction isolated from adipose tissue and modulated uptake of apoptotic adipocytes by macrophages. Despite changes in macrophage abundance and polarity, absence of MBL did not impact systemic insulin resistance. Finally, in humans, lower levels of circulating MBL were accompanied by enhanced macrophage influx in subcutaneous adipose tissue. We propose a novel role for MBL in recognition and clearance of apoptotic adipocytes during obesity.
- Received February 14, 2014.
- Accepted June 26, 2014.
- © 2014 by the American Diabetes Association.
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