Increased expression of fatty acid synthase and acetyl‑CoA carboxylase in the prefrontal cortex and cerebellum in the valproic acid model of autism

Chen,Jianling; Wu,Wei; Fu,Yingmei; Yu,Shunying; Cui,Donghong; Zhao,Min; Du,Yasong; Li,Jijun; Li,Xiaohong

doi:10.3892/etm.2016.3508

Increased expression of fatty acid synthase and acetyl‑CoA carboxylase in the prefrontal cortex and cerebellum in the valproic acid model of autism

Authors:
- Jianling Chen
- Wei Wu
- Yingmei Fu
- Shunying Yu
- Donghong Cui
- Min Zhao
- Yasong Du
- Jijun Li
- Xiaohong Li
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Affiliations: Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, P.R. China, Department of Pathology, Shanghai Pulmonary Hospital, Tongji University, Shanghai 200433, P.R. China, Department of Integrative Medicine on Pediatrics, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, P.R. China
Published online on: July 5, 2016 https://doi.org/10.3892/etm.2016.3508
Pages: 1293-1298
Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The primary aim of the present study was to investigate alterations in enzymes associated with fatty acid synthesis, namely fatty acid synthase (FASN) and acetyl‑CoA carboxylase (ACC), in the prefrontal cortex and cerebellum of the valproic acid (VPA)‑induced animal model of autism. In this model, pregnant rats were given a single intraperitoneal injection of VPA, and prefrontal cortex and cerebellum samples from their pups were analyzed. The results of western blotting and reverse transcription‑quantitative polymerase chain reaction analyses demonstrated that the protein and mRNA expression levels of FASN, ACC and phospho‑ACC (pACC) were increased in the prefrontal cortex and cerebellum of the VPA model of autism. Furthermore, in the prefrontal cortex and cerebellum of the VPA model of autism, AMPK expression is increased, whereas PI3K and Akt expression are unchanged. This suggests that disorder of the phosphatidylinositol‑4,5-bisphosphate 3‑kinase (PI3K)/Akt/FASN and/or adenosine 5'‑monophosphate‑activated protein kinase (AMPK)/ACC pathway may be involved in the pathogenesis of autism. It is hypothesized that fatty acid synthesis participates in autism through PI3K/Akt/FASN and AMPK/ACC pathways.

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