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Updated: May 22, 2026

Parallel Measurement of Circadian Clock Gene Expression and Hormone Secretion in Human Primary Cell Cultures
Published on: November 11, 2016
Nocturnin: at the crossroads of clocks and metabolism
Jeremy J Stubblefield1, Jérémy Terrien, Carla B Green
1Department of Neuroscience, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, NB4.204G, Dallas, TX 75390-9111, USA.
Abstract:
Many aspects of metabolism exhibit daily rhythmicity under the control of endogenous circadian clocks, and disruptions in circadian timing result in dysfunctions associated with the metabolic syndrome. Nocturnin (Noc) is a robustly rhythmic gene that encodes a deadenylase thought to be involved in the removal of polyA tails from mRNAs. Mice lacking the Noc gene display resistance to diet-induced obesity and hepatic steatosis, due in part to reduced lipid trafficking in the small intestine. In addition, Noc appears to play important roles in other tissues and has been implicated in lipid metabolism, adipogenesis, glucose homeostasis, inflammation and osteogenesis. Therefore, Noc is a potential key post-transcriptional mediator in the circadian control of many metabolic processes.
Insights
The circadian clock gene Nocturnin (Noc) regulates metabolism. Mice lacking Noc resist diet-induced obesity, suggesting Noc is a key mediator in circadian metabolic control.
Area of Science:
- Molecular Biology
- Metabolic Research
- Chronobiology
Background:
- Metabolism is regulated by circadian clocks, and disruptions cause metabolic syndrome.
- Nocturnin (Noc) is a rhythmic gene encoding a deadenylase involved in mRNA regulation.
Purpose of the Study:
- To investigate the role of Nocturnin (Noc) in circadian regulation of metabolic processes.
- To understand Noc's function in diet-induced obesity and hepatic steatosis.
Main Methods:
- Analysis of Noc gene function in mouse models.
- Assessment of metabolic parameters including obesity, hepatic steatosis, and lipid trafficking.
Main Results:
- Mice lacking the Noc gene showed resistance to diet-induced obesity and hepatic steatosis.
- Reduced lipid trafficking in the small intestine was observed in Noc-deficient mice.
- Noc's involvement in lipid metabolism, adipogenesis, glucose homeostasis, inflammation, and osteogenesis was implicated.
Conclusions:
- Nocturnin (Noc) is a critical post-transcriptional regulator in the circadian control of metabolism.
- Targeting Noc may offer therapeutic strategies for metabolic disorders like obesity and hepatic steatosis.
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