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
Eva FeldmanUniversity of Michigan