Abstract 696: Surgical Injury Induces Local and Distant Adipose Tissue Browning
Objective: Adipose tissue quantity and quality are strong predictors of vascular function. The adipose organ, which comprises brown, white and beige adipocytes, possesses remarkable plasticity in response to feeding and cold exposure. While surgical procedures constantly traumatize adipose tissue, its impact on adipocyte phenotypes remains to be established.
Approach and Results: We studied the effect of trauma on adipocyte phenotypes one day after sham, incision control, or surgical injury to the left inguinal adipose compartment. We included caloric restriction to control for surgery-associated body temperature changes and weight loss. The cellular and molecular changes in subcutaneous, visceral, interscapular, and perivascular adipose tissue using histology, immunohistochemistry, gene expression and flow cytometry analysis. After one day, surgical trauma stimulated adipose tissue browning at the site of injury (Figure 1) and, importantly, in the contralateral inguinal depot. Browning was not present after incision only, and was independent of surgery-associated body temperature and weight loss. Adipose trauma rapidly recruited monocytes to the injured site and promoted alternatively activated macrophages. Conversely, PDGF receptor-positive beige progenitors were reduced. Finally, eight hours after adipose injury, mice had increased levels of circulating norepinephrine, which correlated with reduced lipid content and adipocytes size.
Conclusions: In this study, we identify adipose trauma as an unexpected driver of adipose tissue browning, holding important implications for the biologic response to injury.
Author Disclosures: A. Longchamp: Research Grant; Significant; Swiss National Science Foundation (P1LAP3_158895). M. Tao: None. A. Bartelt: None. K. Ding: None. L. Lynch: None. C. Hine: None. J. Corpataux: None. B. Kristal: None. J. Mitchell: Research Grant; Significant; NIH (NIDDK DK090629; NIA AG036712). C. Ozaki: Research Grant; Significant; American Heart Association (12GRNT9510001, 12GRNT1207025).
This research has received full or partial funding support from the American Heart Association.
- © 2015 by American Heart Association, Inc.