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Article: Activation of hypothalamic RIP‐Cre neurons promotes beiging of WAT via sympathetic nervous system

TitleActivation of hypothalamic RIP‐Cre neurons promotes beiging of WAT via sympathetic nervous system
Authors
KeywordsAMPK
Beiging
Hypothalamus
Obesity
Sympathetic nervous system
Issue Date2018
PublisherNature Publishing Group. The Journal's web site is located at http://www.emboreports.org
Citation
EMBO Reports, 2018, v. 19 n. 4, article no. e44977 How to Cite?
AbstractActivation of brown adipose tissue (BAT) and beige fat by cold increases energy expenditure. Although their activation is known to be differentially regulated in part by hypothalamus, the underlying neural pathways and populations remain poorly characterized. Here, we show that activation of rat‐insulin‐promoter‐Cre (RIP‐Cre) neurons in ventromedial hypothalamus (VMH) preferentially promotes recruitment of beige fat via a selective control of sympathetic nervous system (SNS) outflow to subcutaneous white adipose tissue (sWAT), but has no effect on BAT. Genetic ablation of APPL2 in RIP‐Cre neurons diminishes beiging in sWAT without affecting BAT, leading to cold intolerance and obesity in mice. Such defects are reversed by activation of RIP‐Cre neurons, inactivation of VMH AMPK, or treatment with a β3‐adrenergic receptor agonist. Hypothalamic APPL2 enhances neuronal activation in VMH RIP‐Cre neurons and raphe pallidus, thereby eliciting SNS outflow to sWAT and subsequent beiging. These data suggest that beige fat can be selectively activated by VMH RIP‐Cre neurons, in which the APPL2–AMPK signaling axis is crucial for this defending mechanism to cold and obesity.
Persistent Identifierhttp://hdl.handle.net/10722/256350
ISSN
2019 Impact Factor: 7.497
2015 SCImago Journal Rankings: 4.291
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, B-
dc.contributor.authorLi, A-
dc.contributor.authorLi, X-
dc.contributor.authorHo, WL-
dc.contributor.authorWu, D-
dc.contributor.authorWang, X-
dc.contributor.authorLiu, Z-
dc.contributor.authorWu, K-
dc.contributor.authorYau, S-
dc.contributor.authorXu, A-
dc.contributor.authorCheng, K-
dc.date.accessioned2018-07-20T06:33:16Z-
dc.date.available2018-07-20T06:33:16Z-
dc.date.issued2018-
dc.identifier.citationEMBO Reports, 2018, v. 19 n. 4, article no. e44977-
dc.identifier.issn1469-221X-
dc.identifier.urihttp://hdl.handle.net/10722/256350-
dc.description.abstractActivation of brown adipose tissue (BAT) and beige fat by cold increases energy expenditure. Although their activation is known to be differentially regulated in part by hypothalamus, the underlying neural pathways and populations remain poorly characterized. Here, we show that activation of rat‐insulin‐promoter‐Cre (RIP‐Cre) neurons in ventromedial hypothalamus (VMH) preferentially promotes recruitment of beige fat via a selective control of sympathetic nervous system (SNS) outflow to subcutaneous white adipose tissue (sWAT), but has no effect on BAT. Genetic ablation of APPL2 in RIP‐Cre neurons diminishes beiging in sWAT without affecting BAT, leading to cold intolerance and obesity in mice. Such defects are reversed by activation of RIP‐Cre neurons, inactivation of VMH AMPK, or treatment with a β3‐adrenergic receptor agonist. Hypothalamic APPL2 enhances neuronal activation in VMH RIP‐Cre neurons and raphe pallidus, thereby eliciting SNS outflow to sWAT and subsequent beiging. These data suggest that beige fat can be selectively activated by VMH RIP‐Cre neurons, in which the APPL2–AMPK signaling axis is crucial for this defending mechanism to cold and obesity.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.emboreports.org-
dc.relation.ispartofEMBO Reports-
dc.subjectAMPK-
dc.subjectBeiging-
dc.subjectHypothalamus-
dc.subjectObesity-
dc.subjectSympathetic nervous system-
dc.titleActivation of hypothalamic RIP‐Cre neurons promotes beiging of WAT via sympathetic nervous system-
dc.typeArticle-
dc.identifier.emailWang, B: baile612@hku.hk-
dc.identifier.emailHo, WL: hwl2002@hku.hk-
dc.identifier.emailWang, X: xqwang@hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.authorityHo, WL=rp00259-
dc.identifier.authorityWang, X=rp00507-
dc.identifier.authorityXu, A=rp00485-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.15252/embr.201744977-
dc.identifier.pmid29467283-
dc.identifier.pmcidPMC5891405-
dc.identifier.scopuseid_2-s2.0-85042182991-
dc.identifier.hkuros285912-
dc.identifier.volume19-
dc.identifier.issue4-
dc.identifier.spagearticle no. e44977-
dc.identifier.epagearticle no. e44977-
dc.identifier.isiWOS:000429540900008-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl1469-221X-

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