Send to:

Choose Destination
See comment in PubMed Commons below
Curr Opin Clin Nutr Metab Care. 2014 Nov;17(6):503-8. doi: 10.1097/MCO.0000000000000102.

Is the heat surrounding adipose tissue mitochondria warranted?

Author information

  • 1aMetabolism Unit, Shriners Hospitals for Children bDepartment of Surgery, University of Texas Medical Branch cDepartment of Internal Medicine, University of Texas Medical Branch, Galveston, Texas, USA.



Mitochondrial uncoupling proteins uncouple oxidative phosphorylation. The physiological role ascribed to this process is thermoregulation. The metabolic consequence of mitochondrial respiration uncoupled from ATP production is increased substrate oxidation and metabolic rate. The recent discovery of uncoupling protein 1 (UCP1) positive mitochondria in human adipose tissue has rekindled interest in the role of UCP1 in energy balance and metabolic health.


Recently, there have been numerous reports of functional brown adipose tissue in humans. Further, data from cell and murine studies suggest that beige adipocytes can be induced within white adipose tissue. The presence of brown/beige adipocytes with mitochondria expressing UCP1 negatively correlates with adiposity. Further, activation of these adipocytes alters energy balance and substrate metabolism. However, in humans, brown fat content varies significantly. Further, although beige adipocytes can be induced in white adipose tissue of rodents, whether this is also true in humans remains unclear.


The presence of UCP1-positive mitochondria in human adipose tissue represents an exciting therapeutic target for treating obesity and its metabolic complications. Understanding the mechanisms governing brown fat activation will be crucial if the therapeutic potential of UCP1 is to be realized.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins Icon for PubMed Central
    Loading ...
    Write to the Help Desk