Chemistry Faculty Scholarship
Document Type
Article
Publication Date
7-1-2004
Publication Title
International Union of Biochemistry and Molecular Biology Life
Keywords
Adipocyte, lipolysis, Perilipin; Lipid droplets, ADRP, Adipophilin
Abstract
The related disorders of obesity and diabetes are increasing to epidemic proportions. The role of neutral lipid storage and hydrolysis, and hence the adipocyte, is central to understanding this phenomenon. The adipocyte holds the major source of stored energy in the body in the form of triacylglycerols (TAG). It has been known for over 35 years that the breakdown of TAG and release of free (unesterified) fatty acids and glycerol from fat tissue can be regulated by a cAMP-mediated process. However, beyond the initial signaling cascade, the mechanistic details of this lipolytic reaction have remained unclear. Work in recent years has revealed that both hormone-sensitive lipase (HSL), generally thought to be the ratelimiting enzyme, and perilipin, a lipid droplet surface protein, are required for optimal lipid storage and fatty acid release. There are multiple perilipin proteins encoded by mRNA splice variants of a single perilipin gene. The perilipin proteins are polyphosphorylated by protein kinase A and phosphorylation is necessary for translocation of HSL to the lipid droplet and enhanced lipolysis. Hence, the surface of the lipid storage droplet has emerged as a central site of regulation of lipolysis. This review will focus on adipocyte lipolysis with emphasis on hormone signal transduction, lipolytic enzymes, the lipid storage droplet, and fatty acid release from the adipocyte.
First Page
379
Last Page
385
Volume
56
Issue
7
Repository Citation
Tansey, John, "The Central Role of Perilipin A in Lipid Metabolism and Adipocyte Lipolysis" (2004). Chemistry Faculty Scholarship. 4.
https://digitalcommons.otterbein.edu/chem_fac/4
DOI
10.1080/15216540400009968
Version
Post-Print
Peer Reviewed
1
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.