Pharmacologic IRE1/XBP1s activation promotes systemic adaptive remodeling in obesity.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
01 02 2022
Historique:
received: 30 08 2021
accepted: 18 01 2022
entrez: 2 2 2022
pubmed: 3 2 2022
medline: 16 2 2022
Statut: epublish

Résumé

In obesity, signaling through the IRE1 arm of the unfolded protein response exerts both protective and harmful effects. Overexpression of the IRE1-regulated transcription factor XBP1s in liver or fat protects against obesity-linked metabolic deterioration. However, hyperactivation of IRE1 engages regulated IRE1-dependent decay (RIDD) and TRAF2/JNK pro-inflammatory signaling, which accelerate metabolic dysfunction. These pathologic IRE1-regulated processes have hindered efforts to pharmacologically harness the protective benefits of IRE1/XBP1s signaling in obesity-linked conditions. Here, we report the effects of a XBP1s-selective pharmacological IRE1 activator, IXA4, in diet-induced obese (DIO) mice. IXA4 transiently activates protective IRE1/XBP1s signaling in liver without inducing RIDD or TRAF2/JNK signaling. IXA4 treatment improves systemic glucose metabolism and liver insulin action through IRE1-dependent remodeling of the hepatic transcriptome that reduces glucose production and steatosis. IXA4-stimulated IRE1 activation also enhances pancreatic function. Our findings indicate that systemic, transient activation of IRE1/XBP1s signaling engenders multi-tissue benefits that integrate to mitigate obesity-driven metabolic dysfunction.

Identifiants

pubmed: 35105890
doi: 10.1038/s41467-022-28271-2
pii: 10.1038/s41467-022-28271-2
pmc: PMC8807832
doi:

Substances chimiques

Membrane Proteins 0
Transcription Factors 0
X-Box Binding Protein 1 0
Xbp1 protein, mouse 0
Ern2 protein, mouse EC 2.7.1.-
Protein Serine-Threonine Kinases EC 2.7.11.1
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

608

Subventions

Organisme : NIA NIH HHS
ID : R01 AG046495
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK123038
Pays : United States
Organisme : NIDDK NIH HHS
ID : RC2 DK114785
Pays : United States

Informations de copyright

© 2022. The Author(s).

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Auteurs

Aparajita Madhavan (A)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Bernard P Kok (BP)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Bibiana Rius (B)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Julia M D Grandjean (JMD)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Adekunle Alabi (A)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Verena Albert (V)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Ara Sukiasyan (A)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Evan T Powers (ET)

Department of Chemistry, The Scripps Research Institute, La Jolla, CA, 92037, USA.

Andrea Galmozzi (A)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA.
Department of Medicine, University of Wisconsin, Madison, WI, 53705, USA.

Enrique Saez (E)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA. esaez@scripps.edu.

R Luke Wiseman (RL)

Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, 92037, USA. wiseman@scripps.edu.

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Classifications MeSH