RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance

Inflammation and immunity are linked to the onset and development of obesity and metabolic disorders. Pattern recognition receptors (PRRs) are key regulators of inflammation and immunity in response to infection and stress, and they have critical roles in metainflammation. In this study, we investig...

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Autores principales:	Gabsik Yang, Hye Eun Lee, Jin Kyung Seok, Han Chang Kang, Yong-Yeon Cho, Hye Suk Lee, Joo Young Lee
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	pattern-recognition receptors obesity metabolic syndrome metainflammation ER stress Medicine R Pharmacy and materia medica RS1-441
Acceso en línea:	https://doaj.org/article/17ea3425f7f04c8ab5bbb9d4acf0e312
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spelling	oai:doaj.org-article:17ea3425f7f04c8ab5bbb9d4acf0e3122021-11-25T18:39:57ZRIG-I Deficiency Promotes Obesity-Induced Insulin Resistance10.3390/ph141111781424-8247https://doaj.org/article/17ea3425f7f04c8ab5bbb9d4acf0e3122021-11-01T00:00:00Zhttps://www.mdpi.com/1424-8247/14/11/1178https://doaj.org/toc/1424-8247Inflammation and immunity are linked to the onset and development of obesity and metabolic disorders. Pattern recognition receptors (PRRs) are key regulators of inflammation and immunity in response to infection and stress, and they have critical roles in metainflammation. In this study, we investigated whether RIG-I (retinoic acid-inducible gene I)-like receptors were involved in the regulation of obesity-induced metabolic stress in RIG-I knockout (KO) mice fed a high-fat diet (HFD). RIG-I KO mice fed an HFD for 12 weeks showed greater body weight gain, higher fat composition, lower lean body mass, and higher epididymal white adipose tissue (eWAT) weight than WT mice fed HFD. In contrast, body weight gain, fat, and lean mass compositions, and eWAT weight of MDA5 (melanoma differentiation-associated protein 5) KO mice fed HFD were similar to those of WT mice fed a normal diet. RIG-I KO mice fed HFD exhibited more severely impaired glucose tolerance and higher HOMA-IR values than WT mice fed HFD. IFN-β expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-β expression. Our results show that RIG-I deficiency promotes obesity and insulin resistance induced by a high-fat diet, presenting a novel role of RIG-I in the development of obesity and metabolic disorders.Gabsik YangHye Eun LeeJin Kyung SeokHan Chang KangYong-Yeon ChoHye Suk LeeJoo Young LeeMDPI AGarticlepattern-recognition receptorsobesitymetabolic syndromemetainflammationER stressMedicineRPharmacy and materia medicaRS1-441ENPharmaceuticals, Vol 14, Iss 1178, p 1178 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	pattern-recognition receptors obesity metabolic syndrome metainflammation ER stress Medicine R Pharmacy and materia medica RS1-441
spellingShingle	pattern-recognition receptors obesity metabolic syndrome metainflammation ER stress Medicine R Pharmacy and materia medica RS1-441 Gabsik Yang Hye Eun Lee Jin Kyung Seok Han Chang Kang Yong-Yeon Cho Hye Suk Lee Joo Young Lee RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance
description	Inflammation and immunity are linked to the onset and development of obesity and metabolic disorders. Pattern recognition receptors (PRRs) are key regulators of inflammation and immunity in response to infection and stress, and they have critical roles in metainflammation. In this study, we investigated whether RIG-I (retinoic acid-inducible gene I)-like receptors were involved in the regulation of obesity-induced metabolic stress in RIG-I knockout (KO) mice fed a high-fat diet (HFD). RIG-I KO mice fed an HFD for 12 weeks showed greater body weight gain, higher fat composition, lower lean body mass, and higher epididymal white adipose tissue (eWAT) weight than WT mice fed HFD. In contrast, body weight gain, fat, and lean mass compositions, and eWAT weight of MDA5 (melanoma differentiation-associated protein 5) KO mice fed HFD were similar to those of WT mice fed a normal diet. RIG-I KO mice fed HFD exhibited more severely impaired glucose tolerance and higher HOMA-IR values than WT mice fed HFD. IFN-β expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-β expression. Our results show that RIG-I deficiency promotes obesity and insulin resistance induced by a high-fat diet, presenting a novel role of RIG-I in the development of obesity and metabolic disorders.
format	article
author	Gabsik Yang Hye Eun Lee Jin Kyung Seok Han Chang Kang Yong-Yeon Cho Hye Suk Lee Joo Young Lee
author_facet	Gabsik Yang Hye Eun Lee Jin Kyung Seok Han Chang Kang Yong-Yeon Cho Hye Suk Lee Joo Young Lee
author_sort	Gabsik Yang
title	RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance
title_short	RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance
title_full	RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance
title_fullStr	RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance
title_full_unstemmed	RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance
title_sort	rig-i deficiency promotes obesity-induced insulin resistance
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/17ea3425f7f04c8ab5bbb9d4acf0e312
work_keys_str_mv	AT gabsikyang rigideficiencypromotesobesityinducedinsulinresistance AT hyeeunlee rigideficiencypromotesobesityinducedinsulinresistance AT jinkyungseok rigideficiencypromotesobesityinducedinsulinresistance AT hanchangkang rigideficiencypromotesobesityinducedinsulinresistance AT yongyeoncho rigideficiencypromotesobesityinducedinsulinresistance AT hyesuklee rigideficiencypromotesobesityinducedinsulinresistance AT jooyounglee rigideficiencypromotesobesityinducedinsulinresistance
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RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance

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