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