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Table 1 Metabolic phenotypes of clock disorders in mice

From: Circadian rhythms affect bone reconstruction by regulating bone energy metabolism

Mouse/experiment/mutation

Phenotype/mechanism

References

Chronic jet lag (6 h advance/week)

Weight gain

[121]

SCN lesion

Loss of behavioral and molecular rhythms, obesity, hyperphagy

[122]

Light exposure at night

Metabolic and behavioral phase shifts, weight gain

[123, 124]

Per3 knockout

Increased fat mass

[125]

Liver Bmal1 knockout

Hypoglycemia during fasting period

[126]

Pancreas Bmal1 knockout

Hypoinsulinemia

[127]

Cry1/2 double knockout

Loss of behavioral rhythms, hyperinsulinemia

[126, 128]

global Bmal1 knockout

cataract, sarcopenia, arthropathy, and so on

[129]

Clock Δ19 mice and the Clock/Npas2 double knockout

spontaneously calcifying tendons

[130]

Cry

CRY also inhibits the transmission of signals downstream of glucagon receptors, thus affecting the production of glycosomes at specific time

[131]

REV-ERB and HNF6

REV-ERB and HNF6 interact to regulate lipid metabolism

[132]

Npas2−/− mice

Lack nap-type rest periods during the activity Period and cannot be adjusted properly when the eating Time suddenly changes

[133]

Global Per1/2 knockout

Reduced total hepatic triglycerides lever

[134]

Clock, Bmal1, Cry2

Single nucleotide polymorphisms in Cry2, Bmal1 and Clock can alter an individual's risk of type 2 diabetes, abnormal blood lipids

[135,136,137]

Clock mutant, Bmal1−/− and Rev-erbα−/− mice

Hyperlipidemic

Age-related skeletal muscle loss

Fiber-type shift

Impaired muscle regeneration

[129, 138, 139]

liver-specific Bmal1 or

Rev-erbα deletion

Levels of triglycerides, cholesterol and free fatty acids increased during circulation

[140, 141]

Global Clock Δ 19 mutation

Decreased glucose tolerance. Reduced plasma free fatty acids

[142]

Clock mutant

lack the circadian pattern of enterocyte gene expression and lipid absorption

The disruption of myofiber architecture

Reduction in muscle strength. Reduction in mitochondria

[143]

Muscle-specific Bmal1 knockout

Insulin resistance and glucose intolerance

Impaired insulin stimulated glucose uptake

Increased muscle mass and size

Decreased muscle strength

[144]

Per2 knockout or Per2 mutant

No change in muscle mass and lower exercise tolerance

[8]

Rev-erbaα knockout

Disruption of myofiber architecture

Lower exercise capacity

Slight fiber-type shift

[145, 146]