Premium
Browning of subcutaneous white adipose tissue in humans after severe adrenergic stress (1160.5)
Author(s) -
Sidossis Labros,
Porter Craig,
Saraf Manish,
Chao Tony,
Finnerty Celeste,
Chondronikola Maria,
Borsheim Elisabet,
Hawkins Hal,
Herndon David
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1160.5
Subject(s) - brown adipose tissue , medicine , white adipose tissue , thermogenin , endocrinology , adipose tissue , browning , biology , biochemistry
Intriguing new evidence from animal models suggests that white adipose tissue (WAT) can acquire a brown adipose tissue (BAT) phenotype after adrenergic stress. In this study, we investigated whether the WAT of humans has the capacity to adopt a BAT‐like phenotype (browning of WAT). Subcutaneous WAT samples were collected from 20 severely burned children (early group [8±4 days post injury] or late group [37±25 days]) and 6 healthy children (control group). Morphologic assessment of WAT from the late burn group showed numerous multilocular adipocytes that stained positive for uncoupling protein 1 (UCP1). UCP1 protein content was significantly higher in the late burn group compared to healthy controls (2.72±0.31 vs. 22.88±4.45 ng/mg, P<0.001) and the early burn group (6.88±1.39 vs. 22.88±4.45 ng/mg, P<0.01). Likewise, coupled and uncoupled mitochondrial respiration in the late burn group were 3‐fold and 4‐fold greater, respectively compared to the control group (P<0.01) and the maximum activity of citrate synthase (a proxy for mitochondrial content) of the late group was 3.7‐fold (P<0.001) higher than that in the control group. These findings sugges that the observed changes in WAT are functionally significant. To the best of our knowledge, this is the first evidence of the browning of subcutaneous WAT in humans. Our data highlight the role of WAT as a potential regulator of energy balance and metabolic control in humans. Grant Funding Source : Supported by NIH P50‐GM60338, R01‐GM05668, and Shriners Hospitals for Children (84090, 84080)