Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice

Overnutrition engenders the expansion of adipose tissue and the accumulation of immune cells, in particular, macrophages, in the adipose tissue, leading to chronic low-grade inflammation and insulin resistance. In obesity, several proinflammatory subpopulations of adipose tissue macrophages (ATMs) i...

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Main Authors: Dan Wu, Venkateswararao Eeda, Zahra Maria, Komal Rawal, Audrey Wang, Oana Herlea-Pana, Ram Babu Undi, Hui-Ying Lim, Weidong Wang
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2025-04-01
Series:eLife
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Online Access:https://elifesciences.org/articles/100581
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author Dan Wu
Venkateswararao Eeda
Zahra Maria
Komal Rawal
Audrey Wang
Oana Herlea-Pana
Ram Babu Undi
Hui-Ying Lim
Weidong Wang
author_facet Dan Wu
Venkateswararao Eeda
Zahra Maria
Komal Rawal
Audrey Wang
Oana Herlea-Pana
Ram Babu Undi
Hui-Ying Lim
Weidong Wang
author_sort Dan Wu
collection DOAJ
description Overnutrition engenders the expansion of adipose tissue and the accumulation of immune cells, in particular, macrophages, in the adipose tissue, leading to chronic low-grade inflammation and insulin resistance. In obesity, several proinflammatory subpopulations of adipose tissue macrophages (ATMs) identified hitherto include the conventional ‘M1-like’ CD11C-expressing ATM and the newly discovered metabolically activated CD9-expressing ATM; however, the relationship among ATM subpopulations is unclear. The ER stress sensor inositol-requiring enzyme 1α (IRE1α) is activated in the adipocytes and immune cells under obesity. It is unknown whether targeting IRE1α is capable of reversing insulin resistance and obesity and modulating the metabolically activated ATMs. We report that pharmacological inhibition of IRE1α RNase significantly ameliorates insulin resistance and glucose intolerance in male mice with diet-induced obesity. IRE1α inhibition also increases thermogenesis and energy expenditure, and hence protects against high fat diet-induced obesity. Our study shows that the ‘M1-like’ CD11c+ ATMs are largely overlapping with but yet non-identical to CD9+ ATMs in obese white adipose tissue. Notably, IRE1α inhibition diminishes the accumulation of obesity-induced metabolically activated ATMs and ‘M1-like’ ATMs, resulting in the curtailment of adipose inflammation and ensuing reactivation of thermogenesis, without augmentation of the alternatively activated M2 macrophage population. Our findings suggest the potential of targeting IRE1α for the therapeutic treatment of insulin resistance and obesity.
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spelling doaj-art-7ccb9e6a7fe94c1fa7f3953b71e812cb2025-08-20T02:13:06ZengeLife Sciences Publications LtdeLife2050-084X2025-04-011310.7554/eLife.100581Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese miceDan Wu0https://orcid.org/0009-0002-8389-6107Venkateswararao Eeda1https://orcid.org/0000-0003-2740-047XZahra Maria2https://orcid.org/0000-0002-7279-3279Komal Rawal3https://orcid.org/0000-0001-6707-3392Audrey Wang4https://orcid.org/0009-0005-4736-5634Oana Herlea-Pana5https://orcid.org/0000-0002-3235-6795Ram Babu Undi6https://orcid.org/0000-0001-5061-7066Hui-Ying Lim7https://orcid.org/0000-0001-8084-6337Weidong Wang8https://orcid.org/0000-0003-3619-0953Department of Genetics, Heersink School of Medicine, UAB Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, United States; Department of Medicine, Division of Endocrinology, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesIndian Springs School, Pelham, United StatesDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesDepartment of Physiology, Harold Hamm Diabetes Center, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesDepartment of Genetics, Heersink School of Medicine, UAB Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, United States; Department of Physiology, Harold Hamm Diabetes Center, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesDepartment of Genetics, Heersink School of Medicine, UAB Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, United States; Department of Medicine, Division of Endocrinology, The University of Oklahoma Health Sciences Center, Oklahoma City, United StatesOvernutrition engenders the expansion of adipose tissue and the accumulation of immune cells, in particular, macrophages, in the adipose tissue, leading to chronic low-grade inflammation and insulin resistance. In obesity, several proinflammatory subpopulations of adipose tissue macrophages (ATMs) identified hitherto include the conventional ‘M1-like’ CD11C-expressing ATM and the newly discovered metabolically activated CD9-expressing ATM; however, the relationship among ATM subpopulations is unclear. The ER stress sensor inositol-requiring enzyme 1α (IRE1α) is activated in the adipocytes and immune cells under obesity. It is unknown whether targeting IRE1α is capable of reversing insulin resistance and obesity and modulating the metabolically activated ATMs. We report that pharmacological inhibition of IRE1α RNase significantly ameliorates insulin resistance and glucose intolerance in male mice with diet-induced obesity. IRE1α inhibition also increases thermogenesis and energy expenditure, and hence protects against high fat diet-induced obesity. Our study shows that the ‘M1-like’ CD11c+ ATMs are largely overlapping with but yet non-identical to CD9+ ATMs in obese white adipose tissue. Notably, IRE1α inhibition diminishes the accumulation of obesity-induced metabolically activated ATMs and ‘M1-like’ ATMs, resulting in the curtailment of adipose inflammation and ensuing reactivation of thermogenesis, without augmentation of the alternatively activated M2 macrophage population. Our findings suggest the potential of targeting IRE1α for the therapeutic treatment of insulin resistance and obesity.https://elifesciences.org/articles/100581obesityadipose tissue macrophageER stressinsulin resistanceadipose remodelingIRE1 alpha
spellingShingle Dan Wu
Venkateswararao Eeda
Zahra Maria
Komal Rawal
Audrey Wang
Oana Herlea-Pana
Ram Babu Undi
Hui-Ying Lim
Weidong Wang
Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
eLife
obesity
adipose tissue macrophage
ER stress
insulin resistance
adipose remodeling
IRE1 alpha
title Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
title_full Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
title_fullStr Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
title_full_unstemmed Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
title_short Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
title_sort targeting ire1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice
topic obesity
adipose tissue macrophage
ER stress
insulin resistance
adipose remodeling
IRE1 alpha
url https://elifesciences.org/articles/100581
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