Subcutaneous white adipose tissue independently regulates burn-induced hypermetabolism via immune-adipose crosstalk.

Cell Rep

Institute of Medical Science, University of Toronto, Toronto, ON M5S 1A8, Canada; David Braley Cardiac, Vascular and Stroke Research Institute, Hamilton, ON L8L 2X2, Canada; Hamilton General Hospital, Hamilton Health Sciences, Hamilton, ON L8L 2X2, Canada; Department of Surgery, McMaster University, Hamilton, ON L8S 4K1, Canada. Electronic address:

Published: January 2024

AI Article Synopsis

  • Severe burns lead to a long-lasting hypermetabolic state, suggesting deeper biological processes are at play.
  • Research indicates that thermogenic adipose tissues contribute to this hypermetabolism, functioning independently of cold stress.
  • Adipose tissue transplantation studies reveal that burn-injured recipients can have their metabolic issues improved by healthy adipose tissue, with potential therapeutic targets identified in immune-adipose interactions via the nicotinic acetylcholine receptor pathway.

Article Abstract

Severe burns induce a chronic hypermetabolic state that persists well past wound closure, indicating that additional internal mechanisms must be involved. Adipose tissue is suggested to be a central regulator in perpetuating hypermetabolism, although this has not been directly tested. Here, we show that thermogenic adipose tissues are activated in parallel to increases in hypermetabolism independent of cold stress. Using an adipose tissue transplantation model, we discover that burn-derived subcutaneous white adipose tissue alone is sufficient to invoke a hypermetabolic response in a healthy recipient mouse. Concomitantly, transplantation of healthy adipose tissue alleviates metabolic dysfunction in a burn recipient. We further show that the nicotinic acetylcholine receptor signaling pathway may mediate an immune-adipose crosstalk to regulate adipose tissue remodeling post-injury. Targeting this pathway could lead to innovative therapeutic interventions to counteract hypermetabolic pathologies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10845122PMC
http://dx.doi.org/10.1016/j.celrep.2023.113584DOI Listing

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