Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2012.06.139
Title: Impaired insulin signaling in an animal model of Niemann-Pick Type C disease
Authors: Ong, Q.-R.
Lim, M.-L.
Chua, C.-C.
Cheung, N.S.
Wong, B.-S. 
Keywords: GSK3beta
Insulin signaling
Niemann-Pick Type C disease
NPC
Issue Date: 3-Aug-2012
Citation: Ong, Q.-R., Lim, M.-L., Chua, C.-C., Cheung, N.S., Wong, B.-S. (2012-08-03). Impaired insulin signaling in an animal model of Niemann-Pick Type C disease. Biochemical and Biophysical Research Communications 424 (3) : 482-487. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2012.06.139
Abstract: Studies have shown similarities between the histopathological characteristics of NPC and Alzheimer's disease (AD) including amyloid and tau pathologies. While dysfunction in insulin signaling was widely detected in AD brain, the function of insulin signaling proteins has not been examined in NPC disease. In this study, we have examined the expression and phosphorylation of proteins linked to the insulin signaling pathway in the brain of 9weeks old NPCnih mice. Our results showed lower expression of insulin receptor substrate 2 (IRS2) in the NPCnih mice, and insulin receptor substrate 1 (IRS1) expression was almost non-detectable in this NPC mouse model. This reduction was associated with the loss of expression for the regulatory p85 subunit of phosphatidylinositol 3-kinase (p85/PI3K). Interestingly, the impairment was observed to link to a greater reduction of Akt phosphorylation at residue T308 than S473. This aberrant Akt phosphorylation could be contributing to lower GSK3β phosphorylation detected in the NPCnih mouse brain. To our knowledge, this is the first report documenting impaired insulin signaling in the brain of a NPC mouse model. © 2012 Elsevier Inc.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/109401
ISSN: 0006291X
DOI: 10.1016/j.bbrc.2012.06.139
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