RRC ID 59463
Author Charmpilas N, Ruckenstuhl C, Sica V, Büttner S, Habernig L, Dichtinger S, Madeo F, Tavernarakis N, Bravo-San Pedro JM, Kroemer G.
Title Acyl-CoA-binding protein (ACBP): a phylogenetically conserved appetite stimulator.
Journal Cell Death Dis
Abstract Recently, we reported that, in mice, hunger causes the autophagy-dependent release of a protein called "acyl-CoA-binding protein" or "diazepam binding inhibitor" (ACBP/DBI) from cells, resulting in an increase in plasma ACBP concentrations. Administration of extra ACBP is orexigenic and obesogenic, while its neutralization is anorexigenic in mice, suggesting that ACBP is a major stimulator of appetite and lipo-anabolism. Accordingly, obese persons have higher circulating ACBP levels than lean individuals, and anorexia nervosa is associated with subnormal ACBP plasma concentrations. Here, we investigated whether ACBP might play a phylogenetically conserved role in appetite stimulation. We found that extracellular ACBP favors sporulation in Saccharomyces cerevisiae, knowing that sporulation is a strategy for yeast to seek new food sources. Moreover, in the nematode Caenorhabditis elegans, ACBP increased the ingestion of bacteria as well as the frequency pharyngeal pumping. These observations indicate that ACBP has a phylogenetically ancient role as a 'hunger factor' that favors food intake.
Volume 11(1)
Pages 7
Published 2020-1-6
DOI 10.1038/s41419-019-2205-x
PII 10.1038/s41419-019-2205-x
PMID 31907349
PMC PMC6944704
MeSH Animals Appetite* Autophagy* Caenorhabditis elegans / metabolism Diazepam Binding Inhibitor / metabolism* Feeding Behavior Phylogeny* Saccharomyces cerevisiae / metabolism* Spores, Fungal / physiology
IF 5.959
Times Cited 4
Resource
C.elegans tm2995 tm2896