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.