Chronic over-nutrition and dysregulation of GSK3 in diseases

FieldValue
dc.contributor.authorLiu, Xunxian
dc.contributor.authorYao, Zemin
dc.date.accessioned2016-11-21T16:12:35Z
dc.date.available2016-11-21T16:12:35Z
dc.date.issued2016-08-04
dc.identifier.citationNutrition & Metabolism. 2016 Aug 04;13(1):49
dc.identifier.urihttp://dx.doi.org/10.1186/s12986-016-0108-8
dc.identifier.urihttp://hdl.handle.net/10393/35422
dc.description.abstractAbstract Loss of cellular response to hormonal regulation in maintaining metabolic homeostasis is common in the process of aging. Chronic over-nutrition may render cells insensitive to such a hormonal regulation owing to overstimulation of certain signaling pathways, thus accelerating aging and causing diseases. The glycogen synthase kinase 3 (GSK3) plays a pivotal role in relaying various extracellular and intracellular regulatory signals critical to cell growth, survival, regeneration, or death. The main signaling pathway regulating GSK3 activity through serine-phosphorylation is the phosphoinositide 3-kinase (PI3K)/phosphoinositide-dependent kinase-1 (PDK1)/Akt relay that catalyzes serine-phosphorylation and thus inactivation of GSK3. In addition, perilipin 2 (PLIN2) has recently been shown to regulate GSK3 activation through direct association with GSK3. This review summarizes current understanding on environmental and nutritional factors contributing to GSK3 regulation (or dysregulation) through the PI3K/PDK1/Akt/GSK3 axis, and highlights the newly discovered role that PLIN2 plays in regulating GSK3 activity and GSK3 downstream pathways.
dc.titleChronic over-nutrition and dysregulation of GSK3 in diseases
dc.typeJournal Article
dc.date.updated2016-11-21T16:12:35Z
dc.language.rfc3066en
dc.rights.holderThe Author(s).
CollectionLibre accès - Publications // Open Access - Publications

Files