Table 1.

Studies using adipocyte-specific clock genes mutant/knockout mice.

Gene Mutation/Knockout	Mice Phenotype	Effect on Circadian Rhythm and Oxidative Stress	Refs
Bmal1−/− driven by aP2 promoter	↑ HFD-induced obesity ↑ HFD-induced adiposity ↑ plasma leptin level ↓ leptin signaling ↓ energy expenditure ↓ polysaturated fatty acids	abolished rhythmic expression of clock and clock-output genes in both BAT and WAT loss of circadian variation in plasma TG, glucose	[120]
ClockΔ19 driven by aP2 promoter	↑ young mortality rate ↓ rate of glucose tolerance	Not mentioned	[121]
Bmal1−/− driven by UCP1	↓ PVAT-induced vasoconstriction	↓ blood pressure during resting phase ↓ angiotensin and angiotensinogen levels in PVAT	[122]

Bmal1, brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1; aP2, adipocyte protein 2; HFD, high fat diet; BAT, brown adipose tissue; WAT, white adipose tissue; TG, triglyceride; Clock, circadian locomotor output cycles kaput; UCP1, uncoupling protein 1; PVAT, perivascular adipose tissue.