ETNPPL modulates hyperinsulinemia-induced insulin resistance through the SIK1/ROS-mediated inactivation of the PI3K/AKT signaling pathway in hepatocytes.


Journal

Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222

Informations de publication

Date de publication:
05 2023
Historique:
revised: 16 02 2023
received: 23 11 2022
accepted: 27 02 2023
medline: 18 5 2023
pubmed: 17 3 2023
entrez: 16 3 2023
Statut: ppublish

Résumé

Hyperinsulinemia is a critical risk factor for the pathogenesis of insulin resistance (IR) in metabolic tissues, including the liver. Ethanolamine phosphate phospholyase (ETNPPL), a newly discovered metabolic enzyme that converts phosphoethanolamine (PEA) to ammonia, inorganic phosphate, and acetaldehyde, is abundantly expressed in liver tissue. Whether it plays a role in the regulation of hyperinsulinemia-induced IR in hepatocytes remains elusive. Here, we established an in vitro hyperinsulinemia-induced IR model in the HepG2 human liver cancer cell line and primary mouse hepatocyte via a high dose of insulin treatment. Next, we overexpressed ETNPPL by using lentivirus-mediated ectopic to investigate the effects of ETNPPL per se on IR without insulin stimulation. To explore the underlying mechanism of ETNPPL mediating hyperinsulinemia-induced IR in HepG2, we performed genome-wide transcriptional analysis using RNA sequencing (RNA-seq) to identify the downstream target gene of ETNPPL. The results showed that ETNPPL expression levels in both mRNA and protein were significantly upregulated in hyperinsulinemia-induced IR in HepG2 and primary mouse hepatocytes. Upon silencing ETNPPL, hyperinsulinemia-induced IR was ameliorated. Under normal conditions without IR in hepatocytes, overexpressing ETNPPL promotes IR, reactive oxygen species (ROS) generation, and AKT inactivation. Transcriptome analysis revealed that salt-inducible kinase 1 (SIK1) is markedly downregulated in the ETNPPL knockdown HepG2 cells. Moreover, disrupting SIK1 prevents ETNPPL-induced ROS accumulation, damage to the PI3K/AKT pathway and IR. Our study reveals that ETNPPL mediates hyperinsulinemia-induced IR through the SIK1/ROS-mediated inactivation of the PI3K/AKT signaling pathway in hepatocyte cells. Targeting ETNPPL may present a potential strategy for hyperinsulinemia-associated metabolic disorders such as type 2 diabetes.

Identifiants

pubmed: 36924049
doi: 10.1002/jcp.30993
doi:

Substances chimiques

Insulin 0
Phosphatidylinositol 3-Kinases EC 2.7.1.-
phosphorylethanolamine 78A2BX7AEU
Protein Serine-Threonine Kinases EC 2.7.11.1
Proto-Oncogene Proteins c-akt EC 2.7.11.1
Reactive Oxygen Species 0
SIK1 protein, human EC 2.7.11.1
Sik1 protein, mouse EC 2.7.11.1
Alanine-glyoxylate transaminase EC 2.6.1.44

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1046-1062

Informations de copyright

© 2023 Wiley Periodicals LLC.

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Auteurs

Xueyi Chen (X)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.

Ping Liu (P)

Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Wei Zhang (W)

Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Xiaofang Li (X)

Department of Gastroenterology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Caihua Wang (C)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.

Feifei Han (F)

Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Wenxuan Liu (W)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.

Yaoyao Huang (Y)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.

Man Li (M)

Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Yujia Li (Y)

Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Xiaomin Sun (X)

Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Xiaobin Fan (X)

Department of Obstetrics and Gynecology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.

Wenqing Li (W)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.

Yuyan Xiong (Y)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.
Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, China.

Lu Qian (L)

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Shaanxi, Xi'an, China.
Department of Endocrinology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, P.R. China.
Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Northwest University, Shaanxi, Xi'an, China.

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