Table 1.

Effects of tissue-specific vs. whole body circadian gene knockouts on adipose tissue.

Gene	WAT	BAT
BMAL1 (whole body)	Increased adiposity but impaired adipogenesis Adipocyte hypertrophy	Increase in BAT mass and heightened cold tolerance [95]
BMAL1 (adipocyte-specific; adipocyte protein 2 [aP2] driver)	WAT expansion and loss of rhythmicity in polyunsaturated fatty acid release, driving arrhythmic eating [79]	Enhanced cold tolerance [100]
BMAL1 (brown adipocyte-specific, perivascular adipose tissue; Ucp1 driver)		Defective angiotensin production in PVAT. Reduced resting blood pressure, resulting in “superdipper” phenotype [101]
ClockΔ19 mutant (whole body)	Increased mass and exaggerated WAT adipocyte hypertrophy on high fat diet [93] Increased adipogenesis in vivo and in cultured adipose-derived stem cells. Upregulation of adipogenic factors due to loss of transcription factor GILZ expression [99] Blunted lipolysis, resulting in loss of rhythmic glycerol and FA release [88]
REV-ERBα (whole body)	More prone to diet-induced increases in fat mass Upregulation of βKlotho and FGF21 signaling in WAT [102]	Blocks neonatal BAT formation due to loss of brown lineage commitment [100] Improves cold tolerance in a zeitgeber-specific manner [83]
REV-ERBα/β (BAT-specific; Ucp1 driver)		Enhanced cold tolerance (via loss of suppression at Srebp1) [103]
PER2 (whole body)	Reduced fat mass, increased oxidative capacity in WAT Increase in adipogenesis-related genes (activation of PPARG targets) [86]
PER3 (whole body)	Increased adipogenesis Increase proliferation of APCs in vivo (SAT) [98]
Nocturnin (NOC) (whole body)	Protection from diet induced obesity, reduced visceral fat [104]	Altered long-term metabolic adaptation in to cold exposure [97]