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Publication
Insulin resistance in the nervous system.
Authors
Kim B, Feldman EL
Submitted By
Eva Feldman on 6/6/2012
Status
Published
Journal
Trends in endocrinology and metabolism: TEM
Year
2012
Date Published
3/1/2012
Volume : Pages
23 : 133 - 141
PubMed Reference
22245457
Abstract
Metabolic syndrome is a cluster of cardiovascular risk factors including
obesity, diabetes and dyslipidemia. Insulin resistance (IR) is at the core of
metabolic syndrome. In adipose tissue and muscle, IR results in decreased
insulin signaling, primarily affecting downstream phosphatidylinositol 3-kinase
(PI3K)/Akt signaling. It was recently proposed that neurons can develop
hyperinsulinemia-induced IR, which in turn results in injury to the peripheral
and central nervous systems and is probably pathogenic in common neurological
disorders such as diabetic neuropathy and Alzheimer's disease (AD). This review
presents evidence indicating that, similarly to insulin-dependent metabolically
active tissues such as fat and muscle, neurons also develop IR and thus cannot
respond to the neurotrophic properties of insulin, resulting in neuronal injury,
subsequent dysfunction and disease states.
Investigators with authorship
Name
Institution
Eva Feldman
University of Michigan
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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