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An obesogenic feedforward loop involving ACBP/DBI, GABAA receptors and PPARγ

ABSTRACT: An obesogenic feedforward loop involving ACBP/DBI, GABAA receptors and PPARγ

PROVIDER: PRJNA789314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17241913_1.fastq.gz	Fastqsanger.gz
	SRR17241913_2.fastq.gz	Fastqsanger.gz
	SRR17241914_1.fastq.gz	Fastqsanger.gz
	SRR17241914_2.fastq.gz	Fastqsanger.gz
	SRR17241915_1.fastq.gz	Fastqsanger.gz

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An obesogenic feedforward loop involving ACBP/DBI, GABAA receptors and PPARγ

Project description:Total liver RNA extracts from adult male mice (3 months old, Gabrg2tm1Wul/J +/+ or Gabrg2tm1Wul/J F77I/F77I) subjected to Regular-chow or High-fat diet (regime duration: 4weeks) were analyzed to describe the effect of Gabrg2tm1Wul/J genetic background to obesity-induced transcriptomic alterations.

2023-02-24 | GSE191004 | GEO

An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABA<sub>A</sub> receptor.

Project description:Acyl-coenzyme-A-binding protein (ACBP), also known as a diazepam-binding inhibitor (DBI), is a potent stimulator of appetite and lipogenesis. Bioinformatic analyses combined with systematic screens revealed that peroxisome proliferator-activated receptor gamma (PPARγ) is the transcription factor that best explains the ACBP/DBI upregulation in metabolically active organs including the liver and adipose tissue. The PPARγ agonist rosiglitazone-induced ACBP/DBI upregulation, as well as weight gain, that could be prevented by knockout of Acbp/Dbi in mice. Moreover, liver-specific knockdown of Pparg prevented the high-fat diet (HFD)-induced upregulation of circulating ACBP/DBI levels and reduced body weight gain. Conversely, knockout of Acbp/Dbi prevented the HFD-induced upregulation of PPARγ. Notably, a single amino acid substitution (F77I) in the γ2 subunit of gamma-aminobutyric acid A receptor (GABAAR), which abolishes ACBP/DBI binding to this receptor, prevented the HFD-induced weight gain, as well as the HFD-induced upregulation of ACBP/DBI, GABAAR γ2, and PPARγ. Based on these results, we postulate the existence of an obesogenic feedforward loop relying on ACBP/DBI, GABAAR, and PPARγ. Interruption of this vicious cycle, at any level, indistinguishably mitigates HFD-induced weight gain, hepatosteatosis, and hyperglycemia.

| S-EPMC9016078 | biostudies-literature

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Project description:Acyl coenzyme A binding protein (ACBP), encoded by the diazepam binding protein (DBI) gene, plays a pivotal role in stimulating appetite and lipo-anabolic reactions, showing correlations with laboratory indications of metabolic syndrome in ostensibly healthy individuals. In a screening effort targeting inhibitors of ACBP/DBI expression among distinct neuroendocrine factors, we discovered that glucocorticoids induce ACBP/DBI secretion in cultured cells. In mouse models of iatrogenic Cushing syndrome, antibody-mediated neutralization of ACBP/DBI prevented the metabolic consequences of prolonged glucocorticoid administration. Our findings suggest that a surge in extracellular ACBP/DBI may mediate crucial aspects of Cushing syndrome.

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Knockout of the Acyl CoA binding protein (ACBP) in mice - expression profile from the liver of 21 days old ACBP-/- and +/+ mice.

Project description:The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am 15 ACBP-/- and 15 +/+ control mice divided into 6 groups (KO1, KO2, KO3, WT1, WT2 and WT3) with 5 individuals in each group were used for this study.

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Project description:Total liver RNA extracts from adult female mice (8-week-old) subjected to CRS (chronic restraint stress) or CDDP (cisplatin) induced anorexia with or without ACBP/DBI delivery to investigate the impact of ACBP/DBI on anorexia-induced transcriptomic alterations.

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Knockout of the Acyl CoA binding protein (ACBP) in mice - expression profile from the liver of 21 days old ACBP-/- and +/+ mice.

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Bulk RNA seq data from mice lacking ACBP in brown and white adipose tissue

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PPARγ lipodystrophy mutants reveal intermolecular interactions required for enhancer activation

Project description:The peroxisome proliferator-activated receptor γ (PPARγ) is the master regulator of adipocyte differentiation, and mutations that interfere with PPARγ function cause lipodystrophy. Structural studies indicate that PPARγ domains engage in several intra- and inter-moleuclar interactions; however, how these interactions modulate the ability of PPARγ to activate target genes in a cellular context is currently poorly understood. Here we analysed the transcriptional potential of R212Q and E379K two previously uncharacterised lipodystrophy-associated PPARγ mutants that are located in distinct PPARγ domains but are both predicted to affect intermolecular interactions. Using a combination of biochemical and genome-wide approaches we show that these mutations impair binding to an overlapping subset of enhancers that are less accessible and specifically require PPARγ for chromatin remodeling. Based on these findings we propose a model in which recruitment of PPARγ to chromatin is determined by several intermolecular interfaces. Furthermore, our data exemplify that relatively subtle molecular defects in transcription factors are sufficient to significantly affect enhancer binding and thereby transcriptional output.

2022-09-08 | PXD036589 | Pride

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