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Article: SBP2 deficiency in adipose tissue macrophages drives insulin resistance in obesity

TitleSBP2 deficiency in adipose tissue macrophages drives insulin resistance in obesity
Authors
Issue Date2019
PublisherAmerican Association for the Advancement of Science: Science Advances. The Journal's web site is located at http://www.scienceadvances.org/
Citation
Science Advances, 2019, v. 5 n. 8, article no. eaav0198 How to Cite?
AbstractProinflammatory activation and accumulation of adipose tissue macrophages (ATMs) are associated with increased risk of insulin resistance in obesity. Here, we described the previously unidentified role of selenocysteine insertion sequence-binding protein 2 (SBP2) in maintaining insulin sensitivity in obesity. SBP2 was suppressed in ATMs of diet-induced obese mice and was correlated with adipose tissue inflammation. Loss of SBP2 initiated metabolic activation of ATMs, inducing intracellular reactive oxygen species content and inflammasome, which subsequently promoted IL-1 beta-associated local proliferation and infiltration of proinflammatory macrophages. ATM-specific knockdown of SBP2 in obese mice promoted insulin resistance by increasing fat tissue inflammation and expansion. Reexpression of SBP2 improved insulin sensitivity. Last, an herbal formula that specifically induced SBP2 expression in ATMs can experimentally improve insulin sensitivity. Clinical observation revealed that it improved hyperglycemia in patients with diabetes. This study identified SBP2 in ATMs as a potential target in rescuing insulin resistance in obesity.
Persistent Identifierhttp://hdl.handle.net/10722/274832
ISSN
2017 Impact Factor: 11.511
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, N-
dc.contributor.authorTan, HYH-
dc.contributor.authorLi, S-
dc.contributor.authorWang, DI-
dc.contributor.authorXu, Y-
dc.contributor.authorZhang, C-
dc.contributor.authorXia, W-
dc.contributor.authorChe, CM-
dc.contributor.authorFeng, Y-
dc.date.accessioned2019-09-10T02:29:45Z-
dc.date.available2019-09-10T02:29:45Z-
dc.date.issued2019-
dc.identifier.citationScience Advances, 2019, v. 5 n. 8, article no. eaav0198-
dc.identifier.issn2375-2548-
dc.identifier.urihttp://hdl.handle.net/10722/274832-
dc.description.abstractProinflammatory activation and accumulation of adipose tissue macrophages (ATMs) are associated with increased risk of insulin resistance in obesity. Here, we described the previously unidentified role of selenocysteine insertion sequence-binding protein 2 (SBP2) in maintaining insulin sensitivity in obesity. SBP2 was suppressed in ATMs of diet-induced obese mice and was correlated with adipose tissue inflammation. Loss of SBP2 initiated metabolic activation of ATMs, inducing intracellular reactive oxygen species content and inflammasome, which subsequently promoted IL-1 beta-associated local proliferation and infiltration of proinflammatory macrophages. ATM-specific knockdown of SBP2 in obese mice promoted insulin resistance by increasing fat tissue inflammation and expansion. Reexpression of SBP2 improved insulin sensitivity. Last, an herbal formula that specifically induced SBP2 expression in ATMs can experimentally improve insulin sensitivity. Clinical observation revealed that it improved hyperglycemia in patients with diabetes. This study identified SBP2 in ATMs as a potential target in rescuing insulin resistance in obesity.-
dc.languageeng-
dc.publisherAmerican Association for the Advancement of Science: Science Advances. The Journal's web site is located at http://www.scienceadvances.org/-
dc.relation.ispartofScience Advances-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleSBP2 deficiency in adipose tissue macrophages drives insulin resistance in obesity-
dc.typeArticle-
dc.identifier.emailWang, N: ckwang@hku.hk-
dc.identifier.emailTan, HYH: hyhtan@hku.hk-
dc.identifier.emailLi, S: lishaha@hku.hk-
dc.identifier.emailChe, CM: chemhead@hku.hk-
dc.identifier.emailFeng, Y: yfeng@hku.hk-
dc.identifier.authorityWang, N=rp02075-
dc.identifier.authorityChe, CM=rp00670-
dc.identifier.authorityFeng, Y=rp00466-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1126/sciadv.aav0198-
dc.identifier.pmid31453320-
dc.identifier.scopuseid_2-s2.0-85070925049-
dc.identifier.hkuros304747-
dc.identifier.volume5-
dc.identifier.issue8-
dc.identifier.spagearticle no. eaav0198-
dc.identifier.epagearticle no. eaav0198-
dc.identifier.isiWOS:000481798400005-
dc.publisher.placeUnited States-

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