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Flattened circadian glucocorticoid oscillations cause obesity due to increased lipid turnover and lipid uptake

ABSTRACT: Flattened circadian glucocorticoid oscillations cause obesity due to increased lipid turnover and lipid uptake

PROVIDER: PRJNA837272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19172400_1.fastq.gz	Fastqsanger.gz
	SRR19172400_2.fastq.gz	Fastqsanger.gz
	SRR19172401_1.fastq.gz	Fastqsanger.gz
	SRR19172401_2.fastq.gz	Fastqsanger.gz
	SRR19172402_1.fastq.gz	Fastqsanger.gz

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Flattened circadian glucocorticoid oscillations cause obesity due to increased lipid turnover and lipid uptake

Project description:Chronic stressors flatten circadian glucocorticoid (GC) oscillations, which has been correlated with negative health outcomes including obesity. How such flattened circadian GC oscillations affect metabolism and fat storage remains unknown. Here we investigated the consequences in mice and found that flattening of GC oscillations results not only in body weight gain, mainly due to increases in white fat depot mass, but also leads to hyperinsulinemia and fat accumulation in brown adipose tissue. Global analysis of the transcriptome of WAT and BAT revealed alterations in gene expression dependent on flattened GC oscillations and point to increased lipid turnover and lipid uptake in both fat depots.

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Trem2 Promotes Foamy Macrophage Lipid Uptake and Survival in Atherosclerosis

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Drosophila E78A nuclear receptor regulates intestinal dietary triacylglyceride uptake and systemic lipid levels

Project description:Here we show that the Drosophila nuclear receptor E78A regulates transcription in adult animals facilitating dietary lipid uptake. E78A mutant adults are viable with normal developmental timing, locomotor activity, female fecundity, but have significantly reduced stored triglycerides. This reduction in whole body triglyceride stores appears to originate from the midgut, using neutral lipid stainings we determined lipid levels in the midgut were greatly reduced. Upon examining our RNA-seq analysis we found that a gastric lipase, CG17192, is transcriptionally coordinated by E78A. CG17192 is expressed in an adult, intestinal specific fashion within control flies, and has a human ortholog. Through dietary supplementation and genetic testing we determined that the whole body hypolipidemia seen within E78A mutants is dependent on CG17192 expression within the intestine. Restoration of this lipase in the intestine of mutant flies is sufficient to restore normal lipid levels. Our data support the model that E78A contributes to a transcriptional regulation of the gastric lipase, CG17192, thus directing dietary triglyceride uptake in the adult fly.

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Stomatin modulates adipogenesis through ERK pathway and regulates fatty acid uptake and lipid droplet growth

Project description:Controlling fatty acid uptake, lipid production and storage, and metabolism of lipid droplets (LDs), is closely related to lipid homeostasis, adipocyte hypertrophy and obesity. We report here that stomatin, a major constituent of lipid rafts, participates in adipogenesis and adipocyte maturation by modulating related signaling pathways. In adipocyte-like cells, increased stomatin promotes LD growth or enlargements by facilitating LD-LD fusion, as well as fatty acid uptake from extracellular environment by recruiting effector molecules, such as FAT/CD36 translocase, to lipid rafts to promote internalization of fatty acids. Stomatin transgenic mice fed with high-fat diets exhibit obesity, insulin resistance and hepatic impairments; however, such phenotypes are not seen if feeding the transgenic animals with regular diets. Inhibitions of stomatin by gene knockdown or OB-1 pharmacological treatments inhibit adipogenic differentiation and LD growth through downregulation of PPARγ pathway. Effects of stomatin on PPARγ involve ERK signaling; however, an alternate pathway may also exist. Differential expression analyses by microarray were performed comparing stomatin-knockdown and control 3T3-L1 adipocyte-like cells.

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DNA methylation oscillations at CpG poor enhancers in primed embryonic stem cells [amplicon-Seq]

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2012-02-21 | E-GEOD-31901 | biostudies-arrayexpress

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