bims-ciryme Biomed news
on Circadian rhythms and metabolism
Issue of 2019‒03‒10
two papers selected by
Gabriela Da Silva Xavier
University of Birmingham


  1. Cell Metab. 2019 Feb 18. pii: S1550-4131(19)30063-4. [Epub ahead of print]
    Cedernaes J, Huang W, Ramsey KM, Waldeck N, Cheng L, Marcheva B, Omura C, Kobayashi Y, Peek CB, Levine DC, Dhir R, Awatramani R, Bradfield CA, Wang XA, Takahashi JS, Mokadem M, Ahima RS, Bass J.
      The alignment of fasting and feeding with the sleep/wake cycle is coordinated by hypothalamic neurons, though the underlying molecular programs remain incompletely understood. Here, we demonstrate that the clock transcription pathway maximizes eating during wakefulness and glucose production during sleep through autonomous circadian regulation of NPY/AgRP neurons. Tandem profiling of whole-cell and ribosome-bound mRNAs in morning and evening under dynamic fasting and fed conditions identified temporal control of activity-dependent gene repertoires in AgRP neurons central to synaptogenesis, bioenergetics, and neurotransmitter and peptidergic signaling. Synaptic and circadian pathways were specific to whole-cell RNA analyses, while bioenergetic pathways were selectively enriched in the ribosome-bound transcriptome. Finally, we demonstrate that the AgRP clock mediates the transcriptional response to leptin. Our results reveal that time-of-day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and food acquisition with the sleep/wake state.
    Keywords:  AgRP; Agouti-related protein; RNA sequencing; RNA-seq; RiboTag; SCN; circadian; metabolism; suprachiasmatic nucleus; time-restricted feeding
    DOI:  https://doi.org/10.1016/j.cmet.2019.01.023
  2. Curr Biol. 2019 Feb 11. pii: S0960-9822(19)30098-3. [Epub ahead of print]
    Depner CM, Melanson EL, Eckel RH, Snell-Bergeon JK, Perreault L, Bergman BC, Higgins JA, Guerin MK, Stothard ER, Morton SJ, Wright KP.
      People commonly increase sleep duration on the weekend to recover from sleep loss incurred during the workweek. Whether ad libitum weekend recovery sleep prevents metabolic dysregulation caused by recurrent insufficient sleep is unknown. Here, we assessed sleep, circadian timing, energy intake, weight gain, and insulin sensitivity during sustained insufficient sleep (9 nights) and during recurrent insufficient sleep following ad libitum weekend recovery sleep. Healthy, young adults were randomly assigned to one of three groups: (1) control (CON; 9-h sleep opportunities, n = 8), (2) sleep restriction without weekend recovery sleep (SR; 5-h sleep opportunities, n = 14), and (3) sleep restriction with weekend recovery sleep (WR; insufficient sleep for 5-day workweek, then 2 days of weekend recovery, then 2 nights of insufficient sleep, n = 14). For SR and WR groups, insufficient sleep increased after-dinner energy intake and body weight versus baseline. During ad libitum weekend recovery sleep, participants cumulatively slept ∼1.1 h more than baseline, and after-dinner energy intake decreased versus insufficient sleep. However, during recurrent insufficient sleep following the weekend, the circadian phase was delayed, and after-dinner energy intake and body weight increased versus baseline. In SR, whole-body insulin sensitivity decreased ∼13% during insufficient sleep versus baseline, and in WR, whole-body, hepatic, and muscle insulin sensitivity decreased ∼9%-27% during recurrent insufficient sleep versus baseline. Furthermore, during the weekend, total sleep duration was lower in women versus men, and energy intake decreased to baseline levels in women but not in men. Our findings suggest that weekend recovery sleep is not an effective strategy to prevent metabolic dysregulation associated with recurrent insufficient sleep.
    Keywords:  catch-up sleep; circadian misalignment; diabetes; obesity; overeating; sex differences; sleep deprivation; sleep loss; sleep restriction; timing of food intake
    DOI:  https://doi.org/10.1016/j.cub.2019.01.069