Time of Day Determines Post-Exercise Metabolism in Mouse Adipose Tissue
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ABSTRACT:
PROVIDER: PRJNA819992 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18484637_1.fastq.gz | Fastqsanger.gz | |||
| SRR18484637_2.fastq.gz | Fastqsanger.gz | |||
| SRR18484638_1.fastq.gz | Fastqsanger.gz | |||
| SRR18484638_2.fastq.gz | Fastqsanger.gz | |||
| SRR18484639_1.fastq.gz | Fastqsanger.gz |
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Project description:The circadian clock is a cell-autonomous transcription-translation feedback mechanism that anticipates and adapts physiology and behavior to different phases of the day. A variety of factors including hormones, temperature, food-intake, and exercise can act on tissue-specific peripheral clocks to alter the expression of genes that influence metabolism, all in a time-of-day dependent manner. The aim of this study was to elucidate the effects of exercise timing on adipose tissue metabolism. We performed RNA sequencing on inguinal adipose tissue of mice immediately following maximal exercise or sham treatment at the early rest or early active phase. Only during the early active phase did exercise elicit an immediate increase in serum non-esterified fatty acids. Furthermore, early active phase exercise increased expression of markers of thermogenesis and mitochondrial proliferation in inguinal adipose tissue. In vitro, synchronized 3T3-L1 adipocytes showed a timing-dependent difference in Adrb2 expression, as well as a greater lipolytic activity. Thus, the response of adipose tissue to exercise is time- of-day sensitive and may be partly driven by the circadian clock. To determine the influence of feeding state on the time-of-day response to exercise, we replicated the experiment in 10- hour-fasted early rest phase mice to mimic the early active phase metabolic status. A 10-hour fast led to a similar lipolytic response as observed after active phase exercise, but did not replicate the transcriptomic response, suggesting that the observed changes in gene expression are not driven by feeding status. In conclusion, acute exercise elicits timing-specific effects on adipose tissue to maintain metabolic homeostasis.
2023-01-19 | GSE199429 | GEO
Project description:Circadian rhythms of metabolic, hormonal, and behavioral fluctuations and their alterations can impact health. An important gap in knowledge in the field is whether the time of the day of exercise and the age of onset of exercise exert distinct effects at the level of whole-body adipose tissue and body composition. The goal of the present study was to determine how exercise at different times of the day during adolescence impacts the adipose tissue transcriptome and content in a rodent model. Rats were subjected to one of four conditions during their adolescence: early active phase control or exercise (EAC or EAE; ZT13), and late active phase control or exercise (LAC or LAE; ZT23). The effects of exercise timing were assessed at the level of subcutaneous and visceral adipose tissue transcriptome, body composition, hypothalamic expression of orexigenic and anorexigenic genes, blood serum markers and 24-hour core body temperature patterns. We found that late active phase exercise (ZT23) greatly upregulated pathways of lipid synthesis, glycolysis and NADH shuttles in LAE rats, compared to LAC or EAE. Conversely, LAE rats showed notably lower content of adipose tissue. In addition, LAE rats showed notably increased serum FGF21 levels and other serum markers of glucose metabolism impairment compared to other groups. Finally, LAE rats showed higher post-exercise core body temperature compared to other groups. Our results thus indicate that our exercise protocol induced an unusual effect characterized by enhanced lipid synthesis but reduced adipose tissue content in late active-phase but not early active phase exercise during adolescence.
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Project description:Adipose Energy Homeostasis is the important guarantee to maintain the body's energy balance. Recently, it is reported that, in the adipose cell, Kisspeptins play important role in cell proliferation, differentiation, lipid metabolism and some adipocytokine secretion, so Kisspeptins maybe the novel targets of adipose energy homeostasis regulation. Adipose tissue is the core organs that regulates adipose energy homeostasis. Our early studies observed that there is organizational difference that exercise regulated adipose energy homeostasis, and the response of the Kisspeptins to exercise is closely related to the energy state of the body, so we speculated that Kisspeptins play some important role in the exercise regulated adipose energy homeostasis. Based on the cell experiments to clarify the role of Kisspeptins in regulating adipose energy homeostasis, the role of Kisspeptins in the regulation of adipose energy homeostasis were determined in the adipose tissue of conditioned Kiss1 gene knockout mice of CRISPR/Cas9, then we use the single cell transcriptome sequencing, untargeted proteome and targeted metabolome techniques to further explore and elucidate the possible pathways and mechanisms of Kisspeptins mediated adipose energy homeostasis regulated by exercise.
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Project description:We sought to determine the global transcriptional response to exercise in the heart in a time-of-day dependent manner. To accomplish this, adult male mice (C57Bl/6, ~12 weeks of age) were habituated to treadmill exercise and exposed to a single bout of low-moderate intensity exercise (60 mintue, 10 m/min, 0% grade) at ZT0 (beginning of rest phase) or ZT12 (beginning of active phase). RNA was isolated from whole hearts harvested immediately after exercise (or from sedentary control mice) for RNA-Seq.
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Project description:The circadian clock is a cell-autonomous transcription-translation feedback mechanism that anticipates and adapts physiology and behavior to different phases of the day. A variety of factors including hormones, temperature, food-intake, and exercise can act on tissue-specific peripheral clocks to alter the expression of genes that influence metabolism, all in a time-of-day dependent manner. The aim of this study was to elucidate the effects of exercise timing on adipose tissue metabolism. We performed RNA sequencing on inguinal adipose tissue of mice immediately following maximal exercise or sham treatment at the early rest or early active phase. Only during the early active phase did exercise elicit an immediate increase in serum nonesterified fatty acids. Furthermore, early active phase exercise increased expression of markers of thermogenesis and mitochondrial proliferation in inguinal adipose tissue. In vitro, synchronized 3T3-L1 adipocytes showed a timing-dependent difference in Adrb2 expression, as well as a greater lipolytic activity. Thus, the response of adipose tissue to exercise is time-of-day sensitive and may be partly driven by the circadian clock. To determine the influence of feeding state on the time-of-day response to exercise, we replicated the experiment in 10-h-fasted early rest phase mice to mimic the early active phase metabolic status. A 10-h fast led to a similar lipolytic response as observed after active phase exercise but did not replicate the transcriptomic response, suggesting that the observed changes in gene expression are not driven by feeding status. In conclusion, acute exercise elicits timing-specific effects on adipose tissue to maintain metabolic homeostasis.
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Project description:The regulation of metabolism in peripheral tissues is mediated by pathways that are under circadian control. a bidirectional relationship is evident between the circadian clock and hypoxia-inducible factor-1 α (HIF1α), which is specific to time-of-day exercise. To elucidate the role of HIF1α in driving the divergences in the systemic and skeletal muscle metabolic responses to exercise, a skeletal muscle-specific HIF1α knockout (KO) mouse model was generated. Metabolic phenotyping alongside global transcriptomic profiling was conducted under basal conditions or in response to an acute exercise bout in HIF1α KO and wild-type (WT) mice at the early rest phase (ZT3) or early active phase (ZT15). Our findings demonstrate that HIF1α is dispensable for the metabolic response to exercise at ZT15, but required for an elevation in glycolytic metabolism in response to exercise at ZT3. Specifically, the loss of HIF1α alters the fate of glucose with a shift towards mannose-6-phosphate production observed at ZT3. In addition, the loss of HIF1α alters the transcriptional profile of skeletal muscle specifically at ZT3 with a shift towards oxidative metabolism. HIF1α contributes to regulating the time-of-day exercise response by driving a shift in substrate preference primarily towards glucose oxidation while sparing fatty acid oxidation. This comprehensive metabolic phenotyping of HIF1α KO mice demonstrates that the contribution of HIF1α to the regulation of time-of-day metabolism is dependent on metabolic status and energetic stressors.
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