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Antibody-mediated neutralization of ACBP/DBI has anorexigenic and lipolytic effects.

Abstract
We recently identified acyl coenzyme A-binding protein (ACBP)/diazepam binding inhibitor (DBI) as a novel 'hunger factor': a protein that is upregulated in human or murine obesity and that, if administered to mice, causes hyperphagy, adipogenesis and obesity. Conversely, neutralization of ACBP/DBI by systemic injection of neutralizing monoclonal antibodies or autoantibodies produced after auto-immunization against ACBP/DBI has anorexigenic and lipolytic effects. Thus, neutralization of ACBP/DBI results in reduced food intake subsequent to the activation of anorexigenic neurons and the inactivation of orexigenic neurons in the hypothalamus. Moreover, ACBP/DBI neutralization results into enhanced triglyceride lipolysis in white fat, a surge in free fatty acids in the plasma, enhanced incorporation of glycerol-derived carbon atoms into glucose, as well as an increase in β-oxidation, resulting in a net reduction of fat mass. Importantly, ACBP/DBI neutralization also stimulated an increase in autophagy in various organs, suggesting that it might mediate anti-ageing effects.
AuthorsValentina Sica, Isabelle Martins, Omar Motiño, José M Bravo-San Pedro, Guido Kroemer
JournalAdipocyte (Adipocyte) Vol. 9 Issue 1 Pg. 116-119 (12 2020) ISSN: 2162-397X [Electronic] United States
PMID32157940 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Antibodies
  • Diazepam Binding Inhibitor
Topics
  • Animals
  • Anorexia (metabolism)
  • Antibodies (metabolism)
  • Diazepam Binding Inhibitor (metabolism)
  • Humans
  • Lipolysis

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