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• W4376116677 endingPage "121765" @default.
• W4376116677 startingPage "121765" @default.
• W4376116677 abstract "Circadian rhythms are closely linked to the metabolic network through circadian feedback regulation. The hexosamine biosynthetic pathway (HBP) is a branch of glucose metabolism that affects circadian rhythms through the O-linked N-acetylglucosamine modification (O-GlcNAcylation) of clock proteins. Here, we found out that, among the downstream metabolites regulated by d-glucosamine (GlcN) in HBP salvage pathway, only GlcN is able to induce circadian phase delay both in vitro and in vivo. Mechanistic studies indicated that the phase-shift induced by GlcN is independent of O-GlcNAcylation. Instead, GlcN selectively up-regulates p-AMPK activity, leading to the inhibition of mTOR signaling pathway, and thus down-regulation of p-BMAL1 both in human cell line and mouse tissues. Moreover, GlcN promoted BMAL1 degradation via proteasome pathway. These findings reveal a novel molecular mechanism of GlcN in regulating clock phase and suggest the therapeutic potential of GlcN as new use for an old drug in the future treatment of shift work and circadian misalignment." @default.
• W4376116677 created "2023-05-12" @default.
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• W4376116677 date "2023-07-01" @default.
• W4376116677 modified "2023-09-27" @default.
• W4376116677 title "d-Glucosamine induces circadian phase delay by promoting BMAL1 degradation through AMPK/mTOR pathway" @default.
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• W4376116677 doi "https://doi.org/10.1016/j.lfs.2023.121765" @default.
• W4376116677 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37169147" @default.
• W4376116677 hasPublicationYear "2023" @default.
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