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ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

ABSTRACT: ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

PROVIDER: PRJNA1166092 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30816743_1.fastq.gz	Fastqsanger.gz
	SRR30816743_2.fastq.gz	Fastqsanger.gz
	SRR30816744_1.fastq.gz	Fastqsanger.gz
	SRR30816744_2.fastq.gz	Fastqsanger.gz
	SRR30816745_1.fastq.gz	Fastqsanger.gz

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ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

Project description:Total liver RNA extracts from adult male mice (8 weeks old, C57BL/6) subjected to Methionine and Choline Deficient Diet (regime duration: 6 weeks) and injected with monoclonal anti-ACBP/DBI (2 doses per week from week 4) were determinated to describe the therapeutic effects of neutrali-zation of ACBP/DBI to MASH-induced transcriptomic alterations.

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Project description:We identified ACBP/DBI as a critical regulator in the pathogenesis of hepatocellular carcinoma (HCC), with its inhibition significantly impairing hepatocarcinogenesis in MASH-driven HCC models. To further elucidate the underlying transcriptional mechanisms, we performed spatial transcriptomic analyses using formalin-fixed, paraffin-embedded (FFPE) liver tissues from the following two experimental models: (i) Western diet (WD) and CCl₄-treated mice with tamoxifen-inducible ACBP/DBI knockout (Dbi⁻/⁻ mice), with Dbi⁺/⁺ littermates serving as controls, after a total of 27 weeks; (ii) WD and CCl₄-treated mice immunized with either keyhole limpet hemocyanin (KLH) alone or KLH-ACBP conjugate, after a total of 34 weeks.

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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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Project description:We demonstrated that ACBP/DBI inhibition impaired hepatocarcinogenesis in NASH/MASH-driven HCC models. To further investigate its potential mechanisms at transcriptional level in NASH/MASH-driven HCC models, we performed Bulk RNA-seq analyses with liver tissues from the following three models, namely, (i) WD/CCl4 with tamoxifen inducible ACBP/DBI knout mice (Dbi-/- mice, Dbi+/+ mice as control) for in total 27 weeks; (ii) WD/CCl4 with KLH/KLH-ACBP immunized mice for in total 34 weeks; and (iii) HFD/DEN with KLH/KLH-ACBP immunized miceI for a total of 36 weeks.

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Project description:Total liver RNA extracts from adult male mice (8 weeks old, C57BL/6) injected with monoclonal anti-ACBP/DBI (1 dose per week) and subjected to Methionine and Choline Deficient Diet (regime duration: 4weeks) were analyzed to describe the effect of neutralization of ACBP/DBI to NASH-induced transcriptomic alterations.

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Project description:Supplementation of ACBP/DBI for the Experimental Treatment of Anorexia Nervosa

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Project description:Acyl-CoA binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), is an extracellular checkpoint of autophagy. Here, we report that patients with histologically confirmed metabolic-associated steatohepatitis (MASH) or liver fibrosis exhibit elevated levels of circulating ACBP/DBI protein as compared to non-affected controls. Plasma ACBP/DBI strongly correlated with the NAFLD and FIB4 scores in patients, and these correlations were independent of age and body mass index. We studied the capacity of a monoclonal antibody (mAb) neutralizing mouse ACBP/DBI to combat active liver disease in several mouse models, in which steatohepatitis had been induced by four different protocols, namely, (i) methionine/choline-deficient diet, (ii) Western style diet (WD) alone, (iii) WD combined with the hepatotoxic agent CCl4, and (iv) a combination of CCl4 injections and oral ethanol challenge. Injections of anti-ACBP/DBI mAb attenuated histological, enzymological, metabolomic and transcriptomic signs of liver damage in these four models, hence halting or reducing the progression of non-alcoholic and alcoholic liver disease. Steatosis, inflammation, ballooning and fibrosis responded to ACBP/DBI inhibition at the preclinical level. Altogether, these findings support a causal role of ACBP/DBI in MASH and liver fibrosis, as well as the possibility to therapeutically target ACBP/DBI.

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

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