ArticleCell stress2021
Elevated plasma levels of the appetite-stimulator ACBP/DBI in fasting and obese subjects.
Article in Cell stress, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 6 citations in OpenAlex.
- Dual-Organelle Secretome Conjugation and Organ-Uptake Tracking (DuO-SCOUT) Enables Deep and Sensitive Mapping of the Secreted Proteins.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell death-induced release of the pro-aging protein acyl CoA binding protein (ACBP) into the circulation.Cell death and differentiation · 2026Article
- Identification of ACBP as a potential target in ciliopathic obesity through multi-omics network analysis.Nature communications · 2026Article
- ACBP/DBI Neutralization Stimulates Anticancer Immune Responses by Upregulating Lamin A in T Cells.ImmunoTargets and therapy · 2026Article
- Atlas of expression of acyl CoA binding protein/diazepam binding inhibitor (ACBP/DBI) in human and mouse.Cell death & disease · 2025Article
- Acyl coenzyme A binding protein (ACBP): An aging- and disease-relevant "autophagy checkpoint".Aging cell · 2023Review
- An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABACell death & disease · 2022Article
- Immunization of mice with the self-peptide ACBP coupled to keyhole limpet hemocyanin.STAR protocols · 2022Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic cells release the phylogenetically ancient protein acyl coenzyme A binding protein (ACBP, which in humans is encoded by the gene DBI, diazepam binding inhibitor) upon nutrient deprivation. Accordingly, mice that are starved for one to two days and humans that undergo voluntary fasting for one to three weeks manifest an increase in the plasma concentration of ACBP/DBI. Paradoxically, ACBP/DBI levels also increase in obese mice and humans. Since ACBP/DBI stimulates appetite, this latter finding may explain why obesity constitutes a self-perpetuating state. Here, we present a theoretical framework to embed these findings in the mechanisms of weight control, as well as a bioinformatics analysis showing that, irrespective of the human cell or tissue type, one single isoform of ACBP/DBI (ACBP1) is preponderant (~90% of all DBI transcripts, with the sole exception of the testis, where it is ~70%). Based on our knowledge, we conclude that ACBP1 is subjected to a biphasic transcriptional and post-transcriptional regulation, explaining why obesity and fasting both are associated with increased circulating ACBP1 protein levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.