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Nocturnin: at the crossroads of clocks and metabolism

Journal

TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 23, Issue 7, Pages 326-333

Publisher

ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2012.03.007

Keywords

nocturnin; Ccrn41; circadian; deadenylase; post-transcriptional; metabolic syndrome

Funding

  1. NIGMS NIH HHS [R01 GM076626, R01 GM090247, R01 GM090247-09A1, R01 GM076626-05, R01 GM090247-10] Funding Source: Medline

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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.

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