Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice

ABSTRACT: Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice

PROVIDER: PRJNA564644 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10089847.fastq.gz	Fastqsanger.gz
	SRR10089848.fastq.gz	Fastqsanger.gz
	SRR10089849.fastq.gz	Fastqsanger.gz
	SRR10089850.fastq.gz	Fastqsanger.gz
	SRR10089851.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice.

Project description:Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme for cellular energy metabolism. The aim of the present study was to determine the importance of brown and white adipose tissue (BAT and WAT) NAD+ metabolism in regulating whole-body thermogenesis and energy metabolism. Accordingly, we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice because NAMPT is the rate-limiting NAD+ biosynthetic enzyme. We found ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene programs involved in thermogenesis and mitochondrial function in BAT and a blunted thermogenic (rectal temperature, BAT temperature, and whole-body oxygen consumption) response to acute cold exposure, prolonged fasting, and administration of β-adrenergic agonists (norepinephrine and CL-316243). In addition, the absence of NAMPT in WAT markedly reduced adrenergic-mediated lipolytic activity, likely through inactivation of the NAD+-SIRT1-caveolin-1 axis, which limits an important fuel source fatty acid for BAT thermogenesis. These metabolic abnormalities were rescued by treatment with nicotinamide mononucleotide (NMN), which bypasses the block in NAD+ synthesis induced by NAMPT deficiency. Although BANKO mice, which lack NAMPT in BAT only, had BAT cellular alterations similar to the ANKO mice, BANKO mice had normal thermogenic and lipolytic responses. We also found NAMPT expression in supraclavicular adipose tissue (where human BAT is localized) obtained from human subjects increased during cold exposure, suggesting our finding in rodents could apply to people. These results demonstrate that adipose NAMPT-mediated NAD+ biosynthesis is essential for regulating adaptive thermogenesis, lipolysis, and whole-body energy metabolism.

| S-EPMC6876243 | biostudies-literature

Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice

Project description:We evaluated the effects of NAMPT (nicotinamide phosphoribosyltransferase) knockout on transcriptome in brown adipose tissue (BAT) by analyzing BAT obtained from control (Nampt-flox/flox, F1-F4) and adipocyte-specific Nampt knockout (ANKO, A1-A4) mice.

2019-11-14 | GSE137149 | GEO

Nicotinamide Starvation of Mycobacteria Defective for de novo NAD Biosynthesis

Project description:Mycobacteria can synthesize NAD+ using either the de novo biosynthesis pathway or the salvage pathway. The deletion of the three genes involved specifically in the NAD+ de novo biosynthesis pathway in the human pathogen Mycobacterium tuberculosis had no effect on the growth of the strain in vivo. In contrast, the same deletion in the bovine pathogen Mycobacterium bovis resulted in a strain that could not grow in vivo and could only grow in vitro with substantial nicotinamide supplmentation. This striking difference was attributed to the known defect in the nicotinamidase PncA of M. bovis, since introducing the M. tuberculosis pncA gene into the M. bovis strain defective for de novo NAD+ biosynthesis restored growth in vitro and in vivo. This study demonstrates that NAD+ starvation is a cidal event in mycobacteria and confirms that enzymes common to the de novo and salvage pathways may be good drug targets. We also propose that simultaneously targeting both the salvage and the de novo NAD+ biosynthesis pathways represents a potentially effective way to treat infection with tubercle bacilli. To characterize the lethality induced by nicotinamide starvation transcriptional profiling of the auxotrophs was performed. Triplicate 50 mL cultures of M. tuberculosis and M. bovis Delta nadABC mutants were grown in 7H9 OADC glycerol 0.05% tween broth in 500 mL roller bottles to an OD600nm= 0.1 in a roller incubator at 37Â°C. The cells were washed 1x in PBS and resuspended in 50 mL 7H9 OADC glycerol 0.05% tween broth with or without 20mg/L nicotinamide and returned to the incubator. After 7 days, cultures were harvested. Three biological replicates of each of two species with one dye-flip each

2010-05-14 | E-GEOD-18909 | biostudies-arrayexpress

knock out mutant n575260-NAD biosynthesis in Arabidopsis : role of quinolinate phosphoribosyltransferase

Project description:rs11-01_nad - knock out mutant n575260 - Study of the impact of a deregulation in the NAD concentration in arabidopsis - Study of the biosynthesis of NAD in Arabidopsis. Involvment of QPRTgene using the knock out mutant N575260 from Salk. 2 dye-swap - gene knock out

2012-02-03 | E-GEOD-30976 | biostudies-arrayexpress

down/up regulation of nad biosynthesis in arabidopsis and role of l-aspartate oxidase-Down/up regulation of NAD biosynthesis in Arabidopsis : role of L-Aspartate oxidase

Project description:rs13_01_lao - down/up regulation of nad biosynthesis in arabidopsis and role of l-aspartate oxidase - Study of the biosynthesis of NAD in Arabidopsis. Involvment of L-Aspartate oxidase gene using T-DNA mutant (SAIL1145_B10) and overexpressor lines (promotor 35S, vector PCW162) at the same developmental stage (12 leaves) - Study of the biosynthesis of NAD in Arabidopsis. Involvment of L-Aspartate oxidase gene using T-DNA mutant (SAIL1145_B10) and overexpressor lines (promotor 35S, vector PCW162) at the same developmental stage (12 leaves)

2018-10-01 | GSE120564 | GEO

Down regulation of qptgene in arabidopsis-Regulation of NAD biosynthesis in Arabidopsis : role of quinolinate phosphoribosyltransferase.

Project description:rs11-08_nad2 - down regulation of qptgene in arabidopsis - Study of the biosynthesis of NAD in Arabidopsis. Involvment of QPTgene using the knock out Salk mutant N575260. - Study of the biosynthesis of NAD in Arabidopsis. Involvment of QPTgene using the knock out Salk mutant N575260. 2 dye-swap - normal vs transgenic comparison

2013-08-01 | E-GEOD-49034 | biostudies-arrayexpress

NAD Salvage Supports Serine Biosynthesis

Project description:Maintenance of NAD+ levels by mitochondrial complex I, the NAD+ salvage pathway, and other routes is an important factor in of neurodegenerative disease and cancer. Both the production of NAD+ and the metabolic enzymes that require it as a redox cofactor or substrate differ widely in abundance across cell types and conditions. Disruption in the NAD+ supply thus exerts different effects depending on the cellular NAD+ requirements existing in the cell. Pharmacological depletion of NAD+ is actively being pursued in cancer and other diseases but these effects are not fully understood. Here, we combine quantitative proteomics and metabolomics to understand the consequences of disrupting cellular NAD+ levels and find that inhibiting the NAD+ salvage pathway depletes serine biosynthesis from glucose by impeding the NAD+-dependent protein 3-phosphoglycerate dehydrogenase (PHGDH). Importantly, breast cancers that depend on PHGDH are exquisitely sensitive to blocking the NAD+ salvage pathway. PHGDH, and the rate-limiting enzyme of NAD+ salvage are also correlated in public tumor proteome and transcript datasets. These findings are immediately translatable to the pharmacological inhibition of NAMPT in PHGDH-dependent cancers.

2018-08-14 | PXD007790 | Pride

knock out mutant n575260-NAD biosynthesis in Arabidopsis : role of quinolinate phosphoribosyltransferase

2012-02-03 | GSE30976 | GEO

Nicotinamide Starvation of Mycobacteria Defective for de novo NAD Biosynthesis

Project description:Mycobacteria can synthesize NAD+ using either the de novo biosynthesis pathway or the salvage pathway. The deletion of the three genes involved specifically in the NAD+ de novo biosynthesis pathway in the human pathogen Mycobacterium tuberculosis had no effect on the growth of the strain in vivo. In contrast, the same deletion in the bovine pathogen Mycobacterium bovis resulted in a strain that could not grow in vivo and could only grow in vitro with substantial nicotinamide supplmentation. This striking difference was attributed to the known defect in the nicotinamidase PncA of M. bovis, since introducing the M. tuberculosis pncA gene into the M. bovis strain defective for de novo NAD+ biosynthesis restored growth in vitro and in vivo. This study demonstrates that NAD+ starvation is a cidal event in mycobacteria and confirms that enzymes common to the de novo and salvage pathways may be good drug targets. We also propose that simultaneously targeting both the salvage and the de novo NAD+ biosynthesis pathways represents a potentially effective way to treat infection with tubercle bacilli. To characterize the lethality induced by nicotinamide starvation transcriptional profiling of the auxotrophs was performed. Triplicate 50 mL cultures of M. tuberculosis and M. bovis Delta nadABC mutants were grown in 7H9 OADC glycerol 0.05% tween broth in 500 mL roller bottles to an OD600nm= 0.1 in a roller incubator at 37°C. The cells were washed 1x in PBS and resuspended in 50 mL 7H9 OADC glycerol 0.05% tween broth with or without 20mg/L nicotinamide and returned to the incubator. After 7 days, cultures were harvested.

2010-02-24 | GSE18909 | GEO

Down regulation of qptgene in arabidopsis-Regulation of NAD biosynthesis in Arabidopsis : role of quinolinate phosphoribosyltransferase.

2013-08-01 | GSE49034 | GEO