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Molecular and Cellular Endocrinology
Article . 2012 . Peer-reviewed
License: Elsevier TDM
Data sources: Crossref
versions View all 3 versions

Apelin inhibits adipogenesis and lipolysis through distinct molecular pathways

Authors: Than A.; Cheng Y.; Foh L.-C.; Leow M.K.S.; Lim S.C.; Chuah Y.J.; Kang Y.; +1 Authors

Apelin inhibits adipogenesis and lipolysis through distinct molecular pathways

Abstract

Apelin is an adipokine secreted by adipocytes. Co-expression of apelin and apelin receptor (APJ) in adipocytes implies the autocrine regulations of apelin on adipocyte functions through yet unknown molecular mechanisms. In the present study, we provide evidence that apelin, through its interaction with APJ receptor, inhibits adipogenesis of pre-adipocytes and lipolysis in mature adipocytes. The detailed molecular pathways underlying apelin signaling is proposed based on our experimental observations. Specifically, we show that apelin suppresses adipogenesis through MAPK kinase/ERK dependent pathways. And by preventing lipid droplet fragmentation, apelin inhibits basal lipolysis through AMP kinase dependent enhancement of perilipin expression and inhibits hormone-stimulated acute lipolysis through decreasing perilipin phosphorylation. Apelin induced decrease of free fatty acid release can be attributed to its dual inhibition on adipogenesis and lipolysis. This study suggests that the autocrine signaling of apelin may serve as a novel therapeutic target for obesity and other metabolic disorders.

Keywords

Perilipin, Perilipin-1, MAP Kinase Signaling System, Lipolysis, 610, Gene Expression, Lipid droplet, Mice, Adipokines, 3T3-L1 Cells, Animals, Feedback, Physiological, Flavonoids, Apelin Receptors, Adipogenesis, Lipid Metabolism, PPAR gamma, Autocrine Communication, APJ receptor, CCAAT-Enhancer-Binding Proteins, Apelin, Intercellular Signaling Peptides and Proteins, Mitogen-Activated Protein Kinases, Carrier Proteins

  • BIP!
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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    102
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
102
Top 10%
Top 10%
Top 10%
Green