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 | |
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 | |
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 | |
Clock mutant, Bmal1−/− and Rev-erbα−/− mice | Hyperlipidemic Age-related skeletal muscle loss Fiber-type shift Impaired muscle regeneration | |
liver-specific Bmal1 or Rev-erbα deletion | Levels of triglycerides, cholesterol and free fatty acids increased during circulation | |
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 |