<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13(4)</volume><submitter>Anagnostopoulos G</submitter><funding>Ligue Contre le Cancer</funding><funding>Agence Nationale de la Recherche</funding><funding>Institut National Du Cancer</funding><funding>Fondation Leducq</funding><funding>Fondation pour la Recherche Médicale</funding><pubmed_abstract>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. N</pubmed_abstract><journal>Cell death &amp; disease</journal><pagination>356</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9016078</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABA&lt;sub>A&lt;/sub> receptor.</pubmed_title><pmcid>PMC9016078</pmcid><pubmed_authors>Carbonnier V</pubmed_authors><pubmed_authors>Desdouets C</pubmed_authors><pubmed_authors>Lambertucci F</pubmed_authors><pubmed_authors>Montegut L</pubmed_authors><pubmed_authors>Sandrine G</pubmed_authors><pubmed_authors>Bourgin M</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Kroemer G</pubmed_authors><pubmed_authors>Maiuri MC</pubmed_authors><pubmed_authors>Anagnostopoulos G</pubmed_authors><pubmed_authors>Bravo-San Pedro JM</pubmed_authors><pubmed_authors>Aprahamian F</pubmed_authors><pubmed_authors>Sica V</pubmed_authors><pubmed_authors>Durand S</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Sola MS</pubmed_authors><pubmed_authors>Nirmalathasan N</pubmed_authors><pubmed_authors>Martins I</pubmed_authors><pubmed_authors>Motino O</pubmed_authors><pubmed_authors>Kotta K</pubmed_authors><pubmed_authors>Surdez D</pubmed_authors><pubmed_authors>Donne R</pubmed_authors><pubmed_authors>Delattre O</pubmed_authors></additional><is_claimable>false</is_claimable><name>An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABA&lt;sub>A&lt;/sub> receptor.</name><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. N</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2026-06-18T05:04:45.997Z</modification><creation>2025-02-19T04:20:46.634Z</creation></dates><accession>S-EPMC9016078</accession><cross_references><pubmed>35436993</pubmed><doi>10.1038/s41419-022-04834-5</doi></cross_references></HashMap>