Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786196 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17129400.fastq.gz | Fastqsanger.gz | |||
| SRR17129401.fastq.gz | Fastqsanger.gz | |||
| SRR17129402.fastq.gz | Fastqsanger.gz | |||
| SRR17129403.fastq.gz | Fastqsanger.gz | |||
| SRR17129404.fastq.gz | Fastqsanger.gz |
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Project description:Late eating has been linked to obesity risk. It is not clear whether this is caused by changes in hunger and appetite, energy expenditure or both, nor what molecular pathways in adipose tissues are involved. We conducted a randomized crossover trial to determine the effects of late vs. early meal schedule on the above measures while rigorously controlling for nutrient intake, fasting duration, light exposure, physical activity and sleep opportunity. Late mealtimes doubled the odds of participants reporting hunger (p<0.0001), increased 24-h ghrelin:leptin ratio (p<0.0001) and decreased waketime energy expenditure (p=0.002). Adipose biopsy directional gene expression analyses showed alterations of several pathways attributed to late mealtimes: TGF-β signaling, lipid metabolism, p38 MAPK signaling, modulation of receptor tyrosine kinases, and autophagy, indicating decreased lipolysis/increased lipid synthesis, particularly for phospholipids and membrane-bound lipids. These findings may help develop evidence-based approaches for using appropriate meal timing to prevent and/or treat obesity.
2021-12-06 | GSE190166 | GEO
Project description:Late eating has been linked to obesity risk. It is not clear whether this is caused by changes in hunger and appetite, energy expenditure or both, nor what molecular pathways in adipose tissues are involved. We conducted a randomized crossover trial to determine the effects of late vs. early meal schedule on the above measures while rigorously controlling for nutrient intake, fasting duration, light exposure, physical activity and sleep opportunity. Late mealtimes doubled the odds of participants reporting hunger (p<0.0001), increased 24-h ghrelin:leptin ratio (p<0.0001) and decreased waketime energy expenditure (p=0.002). Adipose biopsy directional gene expression analyses showed alterations of several pathways attributed to late mealtimes: TGF-β signaling, lipid metabolism, p38 MAPK signaling, modulation of receptor tyrosine kinases, and autophagy, indicating decreased lipolysis/increased lipid synthesis, particularly for phospholipids and membrane-bound lipids. These findings may help develop evidence-based approaches for using appropriate meal timing to prevent and/or treat obesity.
2021-12-06 | GSE190167 | GEO
Project description:Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue
| PRJNA786195 | ENA
Project description:Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [array]
| PRJNA786197 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-12-06 | GSE190168 | GEO
Project description:AgRP neurons in the arcuate nucleus of the hypothalamus (ARC) coordinate homeostatic changes in appetite associated with fluctuations in food availability and leptin signaling. Identifying the relevant transcriptional regulatory pathways in these neurons has been a priority, yet such attempts have been stymied due to their low abundance and the rich cellular diversity of the ARC. Here we generated male mouse AgRP neuron-specific transcriptomic and chromatin accessibility profiles during three distinct hunger states of satiety, fasting-induced hunger, and leptin-induced hunger suppression. Cis-regulatory analysis of these integrated datasets enabled the identification of 28 putative hunger-promoting and 29 putative hunger-suppressing transcriptional regulators in AgRP neurons, 16 of which were predicted to be transcriptional effectors of leptin. Within our dataset, Interferon regulatory factor 3 (IRF3) emerged as a leading candidate mediator of leptin-induced hunger-suppression. Gain- and loss-of-function experiments in vivo confirm the role of IRF3 in mediating the acute satiety-evoking effects of leptin in AgRP neurons, while live-cell imaging in vitro indicate that leptin can activate neuronal IRF3 in a cell autonomous manner. Finally, we employ CUT&RUN to uncover direct transcriptional targets of IRF3 in AgRP neurons in vivo. Thus, our findings identify AgRP neuron-expressed IRF3 as a key transcriptional effector of the hunger-suppressing effects of leptin.
2024-04-12 | GSE240484 | GEO
Project description: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 transcription pathway maximizes eating during 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 food acquisition with sleep/wake state. response to leptin. Our results reveal that time-of-day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and food acquisition with sleep/wake state.
2019-03-04 | GSE124693 | GEO
Project description:The combination of decreasing food intake and increasing energy expenditure represents a powerful strategy for counteracting cardiometabolic diseases, such as obesity and type 2 diabetes1. Yet current approaches require conjugating multiple receptor agonists to achieve both effects2–4 and, thus far, no safe energy-expending option has reached the clinic. Here we show that activation of Neurokinin 2 Receptor (NK2R) is sufficient to suppress appetite centrally and increase energy expenditure peripherally. We focused on NK2R after discovering its genetic links to obesity and glucose control. However, therapeutically exploiting NK2R signalling has previously been unattainable because its endogenous ligand, Neurokinin A (NKA), is short-lived and lacks receptor specificity5,6. Therefore, we developed selective, long-acting NK2R agonists, with potential for once-weekly administration in humans. In mice, these agonists elicit weight loss by inducing energy expenditure and non-aversive appetite suppression that circumvents canonical leptin signalling. Additionally, a hyperinsulinemic-euglycemic clamp reveals that NK2R agonism acutely enhances insulin sensitization. In diabetic, obese nonhuman primates, NK2R activation significantly decreases body weight, blood glucose, triglycerides, and cholesterol, and ameliorates insulin resistance. These findings identify a single receptor target that leverages both energy-expending and appetite-suppressing programs to improve energy homeostasis and reverse cardiometabolic dysfunction across species.
2024-11-27 | GSE276735 | GEO
Project description:Appetite is frequently affected in cancer patients, leading to anorexia and consequently insufficient food intake. In this study, we report on hypothalamic gene expression profile of a cancer cachectic mouse model with increased food intake. In this model, mice bearing C26 colon adenocarcinoma have an increased food intake subsequently to the loss of body weight. We hypothesize that in this model, appetite regulating systems in the hypothalamus, which apparently fail in anorexia, are still able to adapt adequately to changes in energy balance. Therefore studying the changes that occur on appetite regulators in the hypothalamus might reveal targets for treatment of cancer-induced eating disorders. By applying transcriptomics, many appetite regulating systems in the hypothalamus could be taken into account, providing an overview of changes that occur in the hypothalamus during tumour growth. We show that hypothalamic expression of orexigenic neuropeptides NPY and AgRP was higher, whereas expression of anorexigenic genes CCK and POMC were lower in TB compared to controls. In addition, serotonin and dopamine signalling pathways were found to be significantly altered in TB mice. Serotonin levels in brain showed to be lower in TB mice compared to control mice, while dopamine levels did not change. Moreover, serotonin levels inversely correlated with food intake. Transcriptomic analysis of the hypothalamus of cachectic TB mice with an increased food intake showed changes in NPY, AgRP and serotonin signalling. Serotonin levels in the brain showed to correlate with changes in food intake. Targeting these systems seems a promising strategy to avoid the development of cancer-induced eating disorders. C26-colon adenocarcinoma cells were subcutaneously inoculated in CDF1 mice. After 20 days, hypothalami were dissected and subjected to gene expression profiling. The total dataset consists of 2 parts; dataset 1, a pilot stuy in which mice were injected with increasing number of tumour cells and pooled samples were arrayed; and dataset 2, the main study in which mice were injected with 1 million tumour cells and samples were individually arrayed.
2013-11-14 | E-GEOD-44080 | biostudies-arrayexpress
Project description:Appetite is frequently affected in cancer patients, leading to anorexia and consequently insufficient food intake. In this study, we report on hypothalamic gene expression profile of a cancer cachectic mouse model with increased food intake. In this model, mice bearing C26 colon adenocarcinoma have an increased food intake subsequently to the loss of body weight. We hypothesize that in this model, appetite regulating systems in the hypothalamus, which apparently fail in anorexia, are still able to adapt adequately to changes in energy balance. Therefore studying the changes that occur on appetite regulators in the hypothalamus might reveal targets for treatment of cancer-induced eating disorders. By applying transcriptomics, many appetite regulating systems in the hypothalamus could be taken into account, providing an overview of changes that occur in the hypothalamus during tumour growth. We show that hypothalamic expression of orexigenic neuropeptides NPY and AgRP was higher, whereas expression of anorexigenic genes CCK and POMC were lower in TB compared to controls. In addition, serotonin and dopamine signalling pathways were found to be significantly altered in TB mice. Serotonin levels in brain showed to be lower in TB mice compared to control mice, while dopamine levels did not change. Moreover, serotonin levels inversely correlated with food intake. Transcriptomic analysis of the hypothalamus of cachectic TB mice with an increased food intake showed changes in NPY, AgRP and serotonin signalling. Serotonin levels in the brain showed to correlate with changes in food intake. Targeting these systems seems a promising strategy to avoid the development of cancer-induced eating disorders. C26-colon adenocarcinoma cells were subcutaneously inoculated in CDF1 mice. After 20 days, hypothalami were dissected and subjected to gene expression profiling. The total dataset consists of 2 parts; dataset 1, a pilot stuy in which mice were injected with increasing number of tumour cells and pooled samples were arrayed; and dataset 2, the main study in which mice were injected with 1 million tumour cells and samples were individually arrayed.
2013-11-14 | E-GEOD-44081 | biostudies-arrayexpress