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A Brain-Melanocortin-Vagus axis mediates adipose tissue expansion independently of energy intake.

ABSTRACT: A Brain-Melanocortin-Vagus axis mediates adipose tissue expansion independently of energy intake.

PROVIDER: PRJNA527312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8735090.fastq.gz	Fastqsanger.gz
	SRR8735100.fastq.gz	Fastqsanger.gz
	SRR8735091.fastq.gz	Fastqsanger.gz
	SRR8735101.fastq.gz	Fastqsanger.gz
	SRR8735092.fastq.gz	Fastqsanger.gz

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A Brain-Melanocortin-Vagus axis mediates adipose tissue expansion independently of energy intake.

Project description:The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing Sympathetic Nervous input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here we demonstrate that obesogenic signals, including reduction of brain-melanocortin signaling or high-fat feeding, actively promote fat mass gain independently of caloric intake via efferent nerve fibers conveyed by the common hepatic branch of the vagus nerve. These signals promote adipose tissue expansion by activating lipogenic program and adipocyte and endothelial cell proliferation independently of insulin action or the sympathetic tone to adipose tissue. These data reveal a novel physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity.

2019-04-18 | GSE128383 | GEO

A Brain-Melanocortin-Vagus Axis Mediates Adipose Tissue Expansion Independently of Energy Intake.

Project description:The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing sympathetic nervous system input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here, we demonstrate that reduction of brain-melanocortin signaling actively promotes fat mass gain by activating the lipogenic program and adipocyte and endothelial cell proliferation in white fat depots independently of caloric intake via efferent nerve fibers conveyed by the common hepatic branch of the vagus nerve. Those vagally regulated obesogenic signals also contribute to the fat mass gain following chronic high-fat diet feeding. These data reveal a physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity.

| S-EPMC6550338 | biostudies-literature

MicroRNA-7 regulates melanocortin circuits involved in mammalian energy homeostasis

Project description:MicroRNA-7 regulates melanocortin circuits involved in mammalian energy homeostasis

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Estrogen Drives Melanocortin Neurons To Reduce Sedentary Behavior

Project description:Estrogen depletion in both rodents and humans leads to inactivity, unhealthy fat accumulation, and metabolic syndrome, underscoring the conserved metabolic benefits of estrogen signaling that inevitably decline with aging. Here, we uncover a hypothalamic node that integrates estrogen and melanocortin-4 receptor (MC4R) signaling to drive episodic bursts in activity prior to ovulation. Skirting the estrogen-dependent gating of this node by CRISPR activation of Mc4r reduces sedentary behavior long-term in both males and females. Our findings expand the impact of MC4R signaling beyond food intake regulation and rationalize reported sex-differences in melanocortin signaling including increased disease severity for women with MC4R-insuffciency. This newly identified hormone-dependent activity node illustrates the potency of estrogen in maintaining an active lifestyle.

2021-03-01 | GSE141434 | GEO

Modulation of brain dead induced inflammation by vagus nerve stimulation

Project description:Because the vagus nerve is implicated in control of inflammation, we investigated if brain death causes impairment of the parasympathetic nervous system, hence contributing to inflammation. Brain death (BD) was induced in rats. Anaesthetised ventilated rats (NBD) served as control. Heart rate variability (HRV) was assessed by ECG. The vagus nerve was electrically stimulated (BD+STIM) during BD. Intestine, kidney, heart and liver were harvested after 6h. Affymetrix chip- analysis was performed on intestinal RNA. Quantitative PCR was performed on all organs. Serum was collected to assess TNFÎ± concentrations. Renal transplantations were performed to address the influence of vagus nerve stimulation on graft outcome. HRV was significantly lower in BD animals. Vagus nerve stimulation inhibited the increase in serum TNFÎ± concentrations and resulted in down-regulation of a multiplicity of pro-inflammatory genes in intestinal tissue. In renal tissue vagal stimulation significantly decreased the expression of E-selectin, IL1Î² and ITGA6. Renal function was significantly better in recipients that received a graft from a BD+STIM donor. Our study demonstrates impairment of the parasympathetic nervous system during BD and inhibition of serum TNFÎ± through vagal stimulation. Vagus nerve stimulation variably affected gene expression in donor organs and improved renal function in recipients. Gene expression in brain dead (BD) induced rat (with and without vagal stimulation) was compared with that of Non brain-dead ventilated control (NBD)

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Mediterranean diet intervention in overweight and obese subjects leads to multiple beneficial shifts in gut microbiome and metabolome independently from energy intake

Project description:Mediterranean diet intervention in overweight and obese subjects leads to multiple beneficial shifts in gut microbiome and metabolome independently from energy intake

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Prepartal energy intake alters blood polymorphonuclear leukocyte transcriptome during the peripartal period in Holstein cows

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2017-03-31 | GSE95677 | GEO

Effects of Maternal Energy Intake on Genomic Imprinting in Fetal Sheep

Project description:Effects of Maternal Energy Intake on Genomic Imprinting in Fetal Sheep

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Vagus nerve inflammation in COVID-19

Project description:To find inflammatory signatures in post mortem vagus nerves of COVID-19 patients in comparisin to non-infected controls.

2023-08-21 | GSE233732 | GEO

Hepatic Vagal Afferents Convey Clock-Dependent Signals to Regulate Circadian Food Intake Patterns

Project description:Circadian desynchrony induced by shiftwork or jetlag is detrimental to metabolic health, but how synchronous or desynchronous signals are transmitted among tissues is unknown. We report that liver molecular clock dysfunction is signaled to the brain through the hepatic vagal afferent nerve (HVAN), leading to altered food intake patterns that are corrected by ablation of the HVAN. Hepatic branch vagotomy also prevents food intake disruptions induced by high-fat diet feeding and reduces body weight gain. Our findings reveal a homeostatic feedback signal that relies on communication between the liver and the brain to control circadian food intake patterns. This identifies the hepatic vagus nerve as a potential therapeutic target for obesity in the setting of chrono-disruption.

2024-12-18 | GSE248462 | GEO

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