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Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity [RNA-seq]

ABSTRACT: Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity [RNA-seq]

PROVIDER: PRJNA625265 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11542200.fastq.gz	Fastqsanger.gz
	SRR11542201.fastq.gz	Fastqsanger.gz
	SRR11542202.fastq.gz	Fastqsanger.gz
	SRR11542203.fastq.gz	Fastqsanger.gz
	SRR11542204.fastq.gz	Fastqsanger.gz

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Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity [RNA-seq]

Project description:Obesity occurs when energy expenditure is outweighed by food intake. Tuberal hypothalamic nuclei, including the arcuate nucleus (ARC), ventromedial nucleus (VMH), and dorsomedial nucleus (DMH), regulate feeding amount as well as energy expenditure. Here we report that mice lacking circadian nuclear receptors REV-ERBa and b in the tuberal hypothalamus (HDKO) gain excessive weight on an obesogenic diet due both to decreased energy expenditure and increased food consumption during the light phase. Moreover, rebound food intake after fasting is markedly increased in HDKO mice. Integrative transcriptomic and cistromic analyses revealed that such disruption in feeding behavior is due to perturbed REV-ERB-dependent leptin signaling in the ARC. Indeed, in vivo leptin sensitivity is impaired in HDKO mice on an obesogenic diet in a circadian manner. Thus, REV-ERBs play a crucial role in hypothalamic regulation of food intake and circadian leptin sensitivity in diet-induced obesity.

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Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity [ChIP-seq]

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Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity

Project description:Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity

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Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity [ChIP-seq]

Project description:Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity [ChIP-seq]

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Hypothalamic REV-ERBs Control Circadian Food Intake and Leptin Sensitivity

Project description:This SuperSeries is composed of the SubSeries listed below.

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Tanycyte-independent control of hypothalamic leptin signaling

Project description:Purpose: 1. Bulk-RNA-Seq was performed to identify tancytye-enriched genes. 2. scRNA-Seq was performed to profile hypothalamic cells following leptin treatment Conclusions: Leptin receptor expression in tanycytes is either absent or undetectably low, that tanycytes do not directly regulate hypothalamic leptin signaling, and that leptin regulates gene expression in diverse hypothalamic cell types through both direct and indirect mechanisms.

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Project description:Pre- and postnatal calorie restriction is associated with postnatal growth restriction, reduced circulating leptin concentrations and perturbed energy balance. Hypothalamic regulation of energy balance demonstrates enhanced orexigenic (NPY, AgRP) and diminished anorexigenic (POMC, CART) neuropeptide expression (PN21) setting the stage for subsequent development of obesity. Leptin replenishment during the early postnatal period (PN2-PN8) led to reversing the hypothalamic orexigenic:anorexigenic neuropeptide ratio at PN21 by only reducing the orexigenic (NPY, AgRP) without affecting the anorexigenic (POMC, CART) neuropeptide expression. This hypothalamic effect was mediated via enhanced leptin receptor (ObRb) signaling that involved increased pSTAT3 but reduced PTP1B. This was further confirmed by an increase in body weight at PN21 in response to intracerebroventricular administration of antisense ObRb oligonucleotides (PN2-PN8). The change in the hypothalamic neuropeptide balance in response to leptin administration caused increased oxygen consumption, carbon dioxide production and physical activity which resulted in increased milk intake (PN14) with no change in body weight. This is in contrast to the reduction in milk intake with no effect on energy expenditure and physical activity observed in controls. We conclude that pre- and postnatal calorie restriction perturbs hypothalamic neuropeptide regulation of energy balance setting the stage for hyperphagia and reduced energy expenditure, hallmarks of obesity. Leptin in turn reverses this phenotype by increasing hypothalamic ObRb signaling (sensitivity) and affecting only the orexigenic arm of the neuropeptide balance.

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