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Deletion of Arntl, a component of the molecular clock, in adipocytes leads to cellular hypertrophy by increasing insulin sensitivity via FGF21
Removing a key cell clock gene in fat cells may cause them to grow larger by increasing insulin response through FGF21
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Abstract
Deletion of the Arntl gene in adipocytes resulted in increased insulin sensitivity and elevated levels in adipose tissue.
- Loss of function in adipocytes is associated with inhibited lipolysis and cellular hypertrophy.
- Elevated expression of Fgf21 in adipose tissue may contribute to metabolic changes observed in adipocyte-specific Arntl deficient mice.
- Double knockout of Arntl and Fgf21 in adipocytes reversed increased insulin sensitivity and adipocyte hypertrophy.
- These findings suggest that BMAL1 influences fat mobilization and insulin signaling through FGF21.
- Disruption of circadian rhythm could be linked to the mechanisms underlying obesity.
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