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Last update 08 May 2025

DBI

Last update 08 May 2025

Basic Info

Synonyms

ACBD1, ACBP, Acyl-CoA-binding protein

+ [5]

Introduction

Binds medium- and long-chain acyl-CoA esters with very high affinity and may function as an intracellular carrier of acyl-CoA esters. It is also able to displace diazepam from the benzodiazepine (BZD) recognition site located on the GABA type A receptor. It is therefore possible that this protein also acts as a neuropeptide to modulate the action of the GABA receptor.

Drugs associated with DBI

WO2023152637

Patent Mining

Target

DBI

Mechanism-

Active Org.

Sorbonne Université [+2]

Originator Org.

Sorbonne Université [+2]

Active Indication

Cardiovascular Diseases [+6]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with DBI

100 Translational Medicine associated with DBI

0 Patents (Medical) associated with DBI

540

Literatures (Medical) associated with DBI

01 Jun 2025·International Dental Journal

Identification and Validation of Ferritinophagy-Related Biomarkers in Periodontitis

Article

Author: Li, Yi-Ming ; Li, Chen-Xi ; Awuti, Gulinuer ; Jureti, Reyila

OBJECTIVEWhile ferritinophagy is believed to play a significant role in the development of periodontitis, the exact mechanisms remain unclear. This study aimed to investigate the biomarkers associated with ferritinophagy in periodontitis using transcriptomic data.METHODSTwo periodontitis-related datasets from Gene Expression Omnibus, GSE10334, and GSE16134, served as the training and validation cohorts, respectively. Additionally, 36 ferritinophagy-related genes (FRGs) were obtained from the GeneCards database. We compared the expression differences of FRGs between the periodontitis and control groups, identifying the different FRGs as candidates. Weighted gene coexpression network analysis (WGCNA) was applied to capture the key modules and modular genes related to periodontitis, utilizing the candidate FRG scores as trait. Then we intersected these with key module genes to identify differentially expressed FRGs. Hub genes were filtered using a protein-protein interaction network. Ultimately, biomarkers were acquired through machine learning, receiver operating characteristic curves, and expression levels. In addition, biomarker-associated immune cells and functional pathways were analysed to predict the upstream regulatory molecules.RESULTSIn total, 18 candidate FRGs showed significant differences between the periodontitis and control groups, and from the protein-protein interaction network, eight hub genes were identified among the 175 differentially expressed FRGs by analysing 1096 differentially expressed genes and 4479 key modular genes. Eventually, ALDH2, diazepam binding inhibitor, HMGCR, OXCT1, and ACAT2 were identified as potential biomarkers through machine learning algorithms, receiver operating characteristic curve analysis, and gene expression assessments. In addition, resting dendritic cells, mast cells, and follicular helper T cells were positively correlated with the five biomarkers (Cor > 0.3 and P < .05). All five biomarkers are involved in the translation initiation pathway, including transcription factors like KLF5 and microRNAs such as hsa-miR-495-3p and hsa-miR-27a-3p. Reverse transcription-quantitative polymerase chain reaction analysis showed that all biomarkers were expressed at low levels in the periodontitis group. However, the differences in expression levels for OXCT1 and ACAT2 between groups were not statistically significant.CONCLUSIONSA total of five ferritinophagy-related biomarkers - ALDH2, diazepam binding inhibitor, HMGCR, OXCT1, and ACAT2 - were screened to explore new treatment options for periodontitis.

01 Jun 2025·Molecular Metabolism

Acyl CoA-binding protein in brown adipose tissue acts as a negative regulator of adaptive thermogenesis

Article

Author: Cereijo, Rubén ; Giralt, Marta ; Rupérez, Celia ; Quesada-López, Tania ; Blasco-Roset, Albert ; Neess, Ditte ; Færgeman, Nils J ; Planavila, Anna ; Mestres-Arenas, Alberto ; Villarroya, Joan ; Godoy-Nieto, Francisco J ; Villarroya, Francesc

OBJECTIVEDefective activity of brown adipose tissue (BAT) is linked to obesity and cardiometabolic diseases. While much is known regarding the biological signals that trigger BAT thermogenesis, relatively little is known about the repressors that may impair BAT function in physiological and pathological settings. Acyl CoA-binding protein (ACBP; also known as diazepam binding inhibitor, DBI) has intracellular functions related to lipid metabolism and can be secreted to act as a circulating regulatory factor that affects multiple organs. Our objective was to determine the role of ACBP in BAT function.METHODSExperimental models based on the targeted inactivation of the Acbp gene in brown adipocytes, both in vitro and in vivo, as well as brown adipocytes treated with recombinant ACBP, were developed and analyzed for transcriptomic and metabolic changes.RESULTSACBP expression and release in BAT are suppressed by noradrenergic cAMP-dependent signals that stimulate thermogenesis. This regulation occurs through gene expression modulation and autophagy-related processes. Mice with targeted ablation of Acbp in brown adipocytes exhibit enhanced BAT thermogenic activity and protection against high-fat diet-induced obesity and glucose intolerance; this is associated with BAT transcriptome changes, including upregulation of BAT thermogenesis-related genes. Treatment of brown adipocytes with exogenous ACBP suppresses oxidative activity, lipolysis, and thermogenesis-related gene expression. ACBP treatment inhibits the noradrenergic-induced phosphorylation of p38 MAP-kinase and CREB, which are major intracellular mediators of brown adipocyte thermogenesis.CONCLUSIONSThe ACBP system acts as a crucial auto regulatory repressor of BAT thermogenesis that responds reciprocally to the noradrenergic induction of BAT activity.

04 Mar 2025·Autophagy

Autophagy-dependent hepatocyte secretion of DBI/ACBP induced by glucocorticoids determines the pathogenesis of Cushing syndrome

Article

Author: Castinetti, Fréderic ; Kroemer, Guido ; Martins, Isabelle ; Pan, Hui ; Tian, Ai-Ling ; Kepp, Oliver

DBI/ACBP is a phylogenetically ancient hormone that stimulates appetite and lipo-anabolism. In response to starvation, DBI/ACBP is secreted through a noncanonical, macroautophagy/autophagy-dependent pathway. The physiological hunger reflex involves starvation-induced secretion of DBI/ACBP from multiple cell types. DBI/ACBP concentrations subsequently increase in extracellular fluids to stimulate food intake. Recently, we observed that glucocorticoids, which are endogenous stress hormones as well as anti-inflammatory drugs, upregulate DBI/ACBP expression at the transcriptional level and stimulate autophagy in hepatocytes, thereby causing a surge in circulating DBI/ACBP levels. Prolonged increase in glucocorticoid concentrations causes an extreme form of metabolic syndrome, dubbed "Cushing syndrome", which is characterized by clinical features including hyperphagia, hyperdipsia, dyslipidemia, hyperinsulinemia, insulin resistance, lipodystrophy, visceral adiposity, steatosis, sarcopenia and osteoporosis. Mice and patients with Cushing syndrome exhibit supraphysiological DBI/ACBP plasma levels. Of note, neutralization of extracellular DBI/ACBP protein with antibodies or mutation of the DBI/ACBP receptor (i.e. the GABRG2 subunit of GABR [gamma-aminobutyric acid type A receptor]) renders mice resistant to the induction of Cushing syndrome. Similarly, knockout of Dbi/Acbp in hepatocytes suppresses the corticotherapy-induced surge in plasma DBI/ACBP concentrations and prevents the manifestation of most of the characteristics of Cushing syndrome. We conclude that autophagy-mediated secretion of DBI/ACBP by hepatocytes constitutes a critical step of the pathomechanism of Cushing syndrome. It is tempting to speculate that stress-induced chronic elevations of endogenous glucocorticoids also compromise human health due to the protracted augmentation of circulating DBI/ACBP concentrations.Abbreviations: DBI/ACBP: diazepam binding inhibitor, acyl-CoA binding protein; GABA: gamma-aminobutyric acid; GABAR: gamma-aminobutyric acid type A receptor; GABRG2: gamma-aminobutyric acid type A receptor subunit gamma2.

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