Table 2: Summary of recent targets for gene manipulation studies designed to impact on brown fat function in adult rodents maintained in a fixed thermal and photoperiodic environment.

Target function, based on brown fat function in the knock outEffect on brown adipose tissueEffect of white adipose tissuePhenotypePrimary mechanismReference


Bone morphogenetic protein (BMP8B)
Normal but reduced thermogenic activity, most apparent during cold exposureNot examinedLower body temperature, increased body mass, and an adaptation amplified with consumption of an HFDModulates SNS activity within BAT[22]
Scaffold protein p62, adipocyte specific knockoutReduced activity and responsiveness to norepinephrineReduced UCP1 within inguinalIncreased body weight and fat mass and an adaptation reduced when fed an HFDActs specifically on mitochondrial function in brown adipocytes and thus thermogenesis [23]


Phosphatase and tensin homolog, conditional knockdownIncreased adipocyte cell sizeIncreased adipocyte cell sizeDespite similar body mass, WAT distribution disorder is apparentBoth brown and white cells may have Myf5+ origins[24]
SERTA domain containing 2 (TRIP-Br2) knock outIncreased thermogenic activity and cold responsivenessDecreased adipocyte cell sizeImproved glucose homeostasis and ability to maintain body temperature during cold exposureModulates fat storage through inhibition of lipolysis, thermogenesis, and oxidative metabolism[25]
Retinaldehyde dehydrogenase
1a, knockout
NoneIncreased UCP1 with a greater response in perigonadal compared with inguinalImproved glucose homeostasis and ability to maintain body temperature during cold exposureInhibits the browning of WAT[26]

BAT: brown adipose tissue; HFD: high fat diet; SNS: sympathetic nervous activity; WAT: white adipose tissue.