Table1.
Gene | Animal Model | Phenotype | Comment | Reference |
---|---|---|---|---|
CLOCK | Clock Δ19 mutant | Hyperphagic Obese | Decreased expression of orexigenic transcripts | 46 |
BMAL1 | Null mice | Arrhythmic feeding | No effect on FAA | 47 |
BMAL1 | VMH specific deletion | Decreased body weight | Affects BAT circadian activity | 56 |
BMAL1 | Liver specific deletion | Hypoglycemia | Arrhythmic expression of hepatic glucose regulatory genes | 102 |
Per1 | S714G mutant | Advanced food intakeIncreased sensitivity to obesity | Feeding uncoupled from energy expenditure | 52 |
Per2 | Null mice(Per2Brdm1) | Absence of diurnal feeding rhythmsImpaired BAT activity | Loss of α-MSH diurnal rhythmsAltered lipid metabolism | 48, 53 |
Cry1/Cry2 | shRNA,Null mice | Absence of diurnal feeding rhythmsHyperglycemia | Feeding behavior rescued by TRF | 50, 148 |
Reverbα | Null mice | Absence of diurnal rhythms of BAT activity | Higher Ucp1 expression in BAT | 54 |
FAA, food anticipatory activity; BAT, brown adipose tissue; α-MSH, α–melanocyte-stimulating hormone; TRF, Time restricted feeding