Time-restricted feeding prevents memory impairments induced by obesogenic diet consumption in mice, in part through hippocampal thyroid hormone signaling.
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ABSTRACT:
PROVIDER: PRJNA1112788 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29067424_1.fastq.gz | Fastqsanger.gz | |||
| SRR29067424_2.fastq.gz | Fastqsanger.gz | |||
| SRR29067425_1.fastq.gz | Fastqsanger.gz | |||
| SRR29067425_2.fastq.gz | Fastqsanger.gz | |||
| SRR29067426_1.fastq.gz | Fastqsanger.gz |
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Project description:Objective: The early consumption of calorie-rich diet disrupts circadian rhythms and has adverse effects on memory, yet the effects of timerestricted feeding (TRF) and the underlying molecular mechanisms are unknown. Here, we set out to identify the behavioral and molecular circadian rhythms disruptions generated by juvenile obesogenic diet consumption and their restoration by TRF in male mice. Methods: Metabolic rhythms were measured by indirect calorimetry and memory performances by behavioral tasks. Hippocampal translatome (pS6_TRAP), enrichment and co-regulated gene network analyses were conducted to identify the molecular pathways involved in memory impairments and their restoration by TRF. Differential exon usage analyses, mass spectrometry and pharmacological intervention were used to confirm thyroid hormone signaling involvement. Results: We show that four weeks of TRF restore the rhythmicity of metabolic parameters and prevents memory impairments in mice fed a high fat-high sucrose (HFS) diet since weaning, independently of body fat levels. Hippocampal translatome and differential exon usage analyses indicate that impaired memory of mice under ad libitum HFS diet is accompanied by reduced thyroid hormone signaling and altered expression of astrocytic genes regulating glutamate neurotransmission. TRF restored the diurnal expression variation of part of these genes and intrahippocampal infusion of T3, the active form of thyroid hormone, rescues memory performances and astrocytic gene expression of ad libitum HFS diet-fed mice. Conclusions: Thus, thyroid hormones contribute to the TRF positive effects on both metabolism and memory in mice fed an obesogenic diet, highlighting this nutritional approach as a powerful tool in addressing obesity brain comorbidities and paving the way for further mechanistic studies on hippocampal thyroid signaling.
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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.
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Project description:High-fat diet (HFD)-induced obesity is a growing epidemic and major health concern. While excessive daytime sleepiness (EDS) is a common symptom of HFD-induced obesity, preliminary findings suggest that reduced wakefulness could be improved with time-restricted feeding (TRF). At present, however, the underlying neural mechanisms remain largely unknown. The paraventricular thalamic nucleus (PVT) plays a role in maintaining wakefulness. We found that chronic HFD impaired the activity of PVT neurons. Notably, inactivation of the PVT was sufficient to reduce and fragment wakefulness during the active phase in lean mice, similar to the sleep-wake alterations observed in obese mice with HFD-induced obesity. On the other hand, enhancing PVT neuronal activity consolidated wakefulness in mice with HFD-induced obesity. We observed that the fragmented wakefulness could be eliminated and reversed by TRF. Furthermore, TRF prevented the HFD-induced disruptions on synaptic transmission in the PVT, in a feeding duration-dependent manner. Collectively, our findings demonstrate that ad libitum access to a HFD results in inactivation of the PVT, which is critical to impaired nocturnal wakefulness and increased sleep, while TRF can prevent and reverse diet-induced PVT dysfunction and excessive sleepiness. We establish a link between TRF and neural activity, through which TRF can potentially serve as a lifestyle intervention against diet/obesity-related EDS.
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