Insulin-signaling abnormalities in drug-naive first-episode schizophrenia: Transduction protein analyses in extracellular vesicles of putative neuronal origin.

ABSTRACT:

Background

Metabolic syndrome and impaired insulin sensitivity may occur as side effects of atypical antipsychotic drugs. However, studies of peripheral insulin resistance using the homeostatic model assessment of insulin resistance (HOMA-IR) or oral glucose tolerance tests (OGTT) suggest that abnormal glucose metabolism is already present in drug-naive first-episode schizophrenia (DNFES). We hypothesized impairments of neuronal insulin signaling in DNFES.

Methods

To gain insight into neuronal insulin-signaling in vivo, we analyzed peripheral blood extracellular vesicles enriched for neuronal origin (nEVs). Phosphorylated insulin signal transduction serine-threonine kinases pS312-IRS-1, pY-IRS-1, pS473-AKT, pS9-GSK3β, pS2448-mTOR, pT389-p70S6K and respective total protein le

SUBMITTER: Kapogiannis D 

PROVIDER: S-EPMC6941668 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature