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 out	Effect on brown adipose tissue	Effect of white adipose tissue	Phenotype	Primary mechanism	Reference
Inhibitory
Bone morphogenetic protein (BMP8B) knockout	Normal but reduced thermogenic activity, most apparent during cold exposure	Not examined	Lower body temperature, increased body mass, and an adaptation amplified with consumption of an HFD	Modulates SNS activity within BAT	[22]
Scaffold protein p62, adipocyte specific knockout	Reduced activity and responsiveness to norepinephrine	Reduced UCP1 within inguinal	Increased body weight and fat mass and an adaptation reduced when fed an HFD	Acts specifically on mitochondrial function in brown adipocytes and thus thermogenesis	[23]
Stimulatory
Phosphatase and tensin homolog, conditional knockdown	Increased adipocyte cell size	Increased adipocyte cell size	Despite similar body mass, WAT distribution disorder is apparent	Both brown and white cells may have Myf5+ origins	[24]
SERTA domain containing 2 (TRIP-Br2) knock out	Increased thermogenic activity and cold responsiveness	Decreased adipocyte cell size	Improved glucose homeostasis and ability to maintain body temperature during cold exposure	Modulates fat storage through inhibition of lipolysis, thermogenesis, and oxidative metabolism	[25]
Retinaldehyde dehydrogenase 1a, knockout	None	Increased UCP1 with a greater response in perigonadal compared with inguinal	Improved glucose homeostasis and ability to maintain body temperature during cold exposure	Inhibits the browning of WAT	[26]

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