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Magnesum Isoglycyrrhizinate augments lipid catabolism via immune-neuro modulation of catecholamine pathways

ABSTRACT: Magnesum Isoglycyrrhizinate augments lipid catabolism via immune-neuro modulation of catecholamine pathways

PROVIDER: PRJNA1144150 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30126906_1.fastq.gz	Fastqsanger.gz
	SRR30126906_2.fastq.gz	Fastqsanger.gz
	SRR30126907_1.fastq.gz	Fastqsanger.gz
	SRR30126907_2.fastq.gz	Fastqsanger.gz
	SRR30126908_1.fastq.gz	Fastqsanger.gz

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Magnesum Isoglycyrrhizinate augments lipid catabolism via immune-neuro modulation of catecholamine pathways

Project description:Glycyrrhetinic acid (GA) and its derivative, magnesium isoglycyrrhizinate, exhibit promising anti-obesity effects through mechanisms that are not fully understood. Here, we showed that GA mitigated white adipose tissue remodeling and diet-induced obesity by enhancing lipid catabolism. GA indirectly promoted adipocyte lipolysis and thermogenesis by modulating catecholamine pathways, facilitated by increased intra-fat sympathetic innervation and reduced protein expression of monoamine oxidase A (MAOA), which degrades norepinephrine. In suit visualization of MAOA identified adipose tissue macrophages (ATMs) as key mediators of intra-fat catecholamine degradation. RNA sequencing of sorted ATMs revealed that GA reduced pro-inflammatory shifts and altered macrophage polarity, preventing activation of the Toll-like receptor 4 (TLR4) signaling pathway, as supported by molecular docking analysis and binding assays. Moreover, the anti-obesity effects of GA were absent in TLR4-deletive mice, which exhibited decreased MAOA protein levels and sensitivity to FUNDC1-mediated mitophagy in ATMs. These findings suggest that GA targets macrophage-sympathetic neuron crosstalk, offering a promising therapeutic approach for obesity by preserving NE availability and promoting lipid catabolism.

2024-10-01 | GSE273958 | GEO

Infiltration of monocyte-derived macrophages perturbs the CNS metabolic landscape, licensing arginine catabolism and augments neuro-inflammation

Project description:Infiltration of monocyte-derived macrophages perturbs the CNS metabolic landscape, licensing arginine catabolism and augments neuro-inflammation

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Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

Project description:While Neanderthals are extinct, fragments of their genome still persist in the genomes of contemporary humans. Here, we show that such Neanderthal-like sequences are not distributed randomly in contemporary human genomes. Specifically, while genome-wide frequency of Neanderthal-like sites is close to 6% in all out-of-Africa populations, genes involved in lipid catabolism contain large excess Neanderthal-like sequences in Europeans (24.3%), but not in Asians (12.4%). While lipid catabolism cannot be assayed in Neanderthals, we took advantage of genetic divergence between human populations, chimpanzees and Neanderthals to predict metabolic divergence expected from the observed excess of Neanderthal gene flow into Europeans. We confirmed predicted changes in lipid catabolism using hydrophobic metabolome measurements in the brain tissue and further linked these metabolic changes to gene expression divergence. 14 human and 6 chimpanzee samples were sequenced.

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Silencing lipid catabolism determines longevity in response to fasting

Project description:Oscillations between lipid anabolism and catabolism allow for long-term preservation of cellular health amid systemic metabolic fluctuations. As a conserved aging determinant, fasting can improve disease outcomes and extend lifespan. Yet, the relative importance of activating lipid catabolism versus its attenuation in fasting-induced longevity remains unclear. The robust adaptability of the soil-dwelling worms, C. elegans, to variable nutrient availability provides an excellent means to better understand how metabolic transitions alter aging trajectories. Here, we show that, rather than activation, the silencing of lipid catabolism upon nutrient replenishment is essential for lifespan extension through fasting. The fasting-responsive nuclear hormone receptor, NHR-49, is pivotal in activating lipid catabolism through β-oxidation. Unlike traditional ligand-regulated nuclear hormone receptors, NHR-49 employs a unique regulatory mechanism that bypasses ligand binding, instead relying on cofactors to mediate its transcriptional attenuation and turnover during times of nutrient stress. Here, we identify casein kinase 1 alpha 1 (KIN-19) as a central regulator of metabolic plasticity and fasting-induced longevity, which attenuates β-oxidation via primed phosphorylation of NHR-49. Overall, cooperative, ligand-independent silencing of this conserved nuclear hormone receptor promotes longevity associated with fasting.

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Silencing lipid catabolism determines longevity in response to fasting [fasting RNA-Seq]

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Silencing lipid catabolism determines longevity in response to fasting

Project description:Silencing lipid catabolism determines longevity in response to fasting

| PRJNA1391526 | ENA

Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

2014-03-31 | GSE45263 | GEO

The class 3 PI3K coordinates autophagy and mitochondrial lipid catabolism by controlling nuclear receptor PPARα

Project description:The class 3 phosphoinositide 3-kinase (PI3K) is required for the lysosomal degradation by autophagy and vesicular trafficking, assuring adaptation to energy shortages. Mitochondrial lipid catabolism is another important energy source. Autophagy and mitochondrial metabolism are transcriptionally controlled by nutrient sensing nuclear receptors. However, it is not known whether the class 3 PI3K contributes to this regulation. Here we show that hepatocyte-specific inactivation of Vps15, the essential regulatory subunit of the class 3 PI3K, results in mitochondrial depletion and a failure to oxidize fatty acids. Mechanistically, the transcriptional activity of Peroxisome Proliferator Activated Receptor alpha (PPARα), a nuclear receptor that orchestrates fatty acid catabolism, is blunted in Vps15-deficient livers. We find PPARα transcriptional repressors Histone Deacetylase 3 (Hdac3) and Nuclear receptor co-repressor 1 (NCoR1) accumulated in Vps15-deficient livers due to defective autophagic flux. Pharmacologic activation of PPARα with a synthetic ligand, re-expression of its co-activator Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α) or inhibition of Hdac3 restored mitochondrial biogenesis and lipid oxidation in Vps15-deficient hepatocytes. These findings reveal a role for the class 3 PI3K and autophagy in transcriptional coordination of mitochondrial metabolism.

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Silencing lipid catabolism determines longevity in response to fasting [fasting RNA-Seq]

Project description:Silencing lipid catabolism determines longevity in response to fasting [fasting RNA-Seq]

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Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

Project description:Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

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