Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied data-independent acquisition proteomics to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for ubiquitylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for succinylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for protein phosphorylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
Project description:Time-restricted eating is emerging as a promising dietary intervention that prevents cardiometabolic disease; however, the molecular mechanisms remain largely unknown. It is generally thought that time-restricted feeding-as it is known in animal studies-reprograms circadian rhythms in peripheral organs including skeletal muscle. Recent studies reported that peripheral organs entrain to time-restricted feeding in a highly diverse tissue-specific manner, which is indicated by the kinetics of the circadian clock in peripheral organs, transcriptome and metabolome. A discrepancy is found in the circadian coherence between rhythmic transcripts and rhythmic metabolites, suggesting the presence of additional regulation at the proteome level. To explore the landscape of rhythmic proteins in skeletal muscle from time-restricted fed mice, we sampled 50 mouse tibialis anterior muscle tissues from 11-week-old C57BL/6J female mice. These mice had been fed day time-restricted feeding for 3 weeks, during which food was accessible between Zeitgeber time (ZT) 0 h and ZT 12 h. Samples were dissected and snap-frozen in liquid nitrogen every two hours starting from ZT0 of the first day to ZT0 of the third day. This sampling scheme covers two complete day/night cycles and has two biological replicates per time point for a total of 25 time points. Next, we performed mass spectrometry-based parallel accumulation–serial fragmentation combined with data-independent acquisition (diaPASEF) quantitative proteomics to analyze these mouse skeletal muscle tissues. Together, we have generated a dataset that provide insights into circadian rhythms of skeletal muscle under the regulation of time-restricted feeding in mice.
Project description:Meal timing is essential in synchronization of circadian rhythms in different organ systems through clock-dependent and -independent mechanisms. The liver is a critical metabolic organ whose circadian clock and transcriptome can be readily reset by meal timing. However, it remains largely unexplored how circadian rhythms in the liver are organized in time-restricted feeding that intervenes meal timing. Here, we applied affinity-purification based shotgun proteomics for N-glycosylation to characterize circadian features associated with day/sleep- (DRF) and night/wake (NRF)-time restricted feeding in nocturnal female mice. The transcriptomics and metabolomics datasets are public (see www.circametdb.org.cn).
Project description:In obesity, misalignment of feeding time with the light/dark environment results in disruption of peripheral circadian clocks. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. Here we show that adipocyte thermogenesis is essential for the healthful metabolic response to time restricted feeding. Genetic enhancement of adipocyte thermogenesis through ablation of Zfp423 attenuates obesity caused by circadian mistimed high fat diet feeding through a mechanism involving creatine metabolism. Circadian control of adipocyte creatine metabolism underlies timing of diet-induced thermogenesis, and enhancement of adipocyte circadian rhythms through overexpression of the clock activator Bmal1 ameliorates metabolic complications during diet induced obesity. These findings establish creatine mediated diet-induced thermogenesis as a bioenergetic mechanism driving metabolic benefits during time-restricted feeding.
Project description:The epidermis is as a highly regenerative barrier protecting organisms from environmental insults, including ultraviolet radiation, the main cause of skin cancer and skin aging. Here we show that time-restricted feeding (RF) shifts the phase and alters the amplitude of the skin circadian clock and affects the expression of approximately 10% of the skin transcriptome. Furthermore, a strikingly large number of skin-expressed genes are acutely regulated by food intake. While the circadian clock is required for daily rhythms in DNA synthesis in epidermal stem cells, RF-induced shifts in clock phase do not alter the phase of DNA synthesis. However, both the expression of the key DNA repair gene Xpa, and the diurnal sensitivity to UVB-induced DNA damage, are altered by RF. Together our findings indicate an unexpected regulation of skin function by time of feeding and emphasize the important link between circadian rhythm, food intake, and skin health.
Project description:Next generation sequencing was used to assess the changes along a diurnal cycle in the transcriptome of Drosophila head, periphery (entire body except the head) or the heart at 3, 5 or 7 weeks of age under ad libitum feeding (ALF) or time-restricted feeding (TRF). Next generation sequencing was used to assess the changes along a diurnal cycle in the transcriptome of Drosophila head, periphery (entire body except the head) or the heart at 3, 5 or 7 weeks of age under ad libitum feeding (ALF) or time-restricted feeding (TRF).
Project description:Circadian rhythm disruption (CD) is associated with dysregulation of glucose homeostasis and Type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates CD-induced metabolic dysfunction. Herein we utilized an approach encompassing analysis of behavioral, physiological, transcriptomic, and single-cell epigenomic effects of CD and consequences of restoration of fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β-cell function and loss of circadian β-cell transcriptional and epigenetic control. In contrast, restoration of fasting/feeding cycle prevented CD-mediated metabolic dysfunction by reestablishing circadian regulation of glucose tolerance, β-cell function, β-cell transcriptional profile, and reestablishment of proline and acidic amino acid-rich basic leucine zipper (PAR-bZIP) transcription factor activity in β-cells. This study provides mechanistic insights into beneficial effects of tRF and its role in prevention of β-cell failure in T2DM.