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Article: Emerging role of autophagy in mediating widespread actions of ADIPOQ/adiponectin

TitleEmerging role of autophagy in mediating widespread actions of ADIPOQ/adiponectin
Authors
Issue Date2015
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/autophagy/index.php
Citation
Autophagy, 2015, v. 11 n. 4, p. 723-724 How to Cite?
AbstractAutophagy can dictate changes in cell metabolism via numerous mechanisms. ADIPOQ/adiponectin has been extensively characterized to have beneficial metabolic effects, both via INS/insulin-sensitizing and INS-independent actions. Our recent work examined the regulation of skeletal muscle autophagy by ADIPOQ and the functional significance. We showed that ADIPOQ directly stimulates autophagic flux in cultured skeletal muscle cells via an AMPK-dependent signaling pathway leading to phosphorylation of ULK1 (Ser555). Pharmacological inhibition of autophagy or overexpressing an inactive mutant of ATG5 to create an autophagy-deficient cell model reduces INS sensitivity. A high-fat diet (HFD) does not induce skeletal muscle autophagy in Adipoq knockout (Ad-KO) mice, whereas it does in wild-type (WT) mice, although ADIPOQ replenishment in Ad-KO mice stimulates autophagy. Changes in skeletal muscle autophagy correlate well with peripheral INS sensitivity and glucose metabolism. Thus, ADIPOQ stimulates autophagic flux in skeletal muscle, which likely represents one important mechanism mediating multiple favorable metabolic effects.
Persistent Identifierhttp://hdl.handle.net/10722/214328
ISSN
2015 Impact Factor: 9.108
2015 SCImago Journal Rankings: 3.916
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorXu, A-
dc.contributor.authorSweeney, G-
dc.date.accessioned2015-08-21T11:15:12Z-
dc.date.available2015-08-21T11:15:12Z-
dc.date.issued2015-
dc.identifier.citationAutophagy, 2015, v. 11 n. 4, p. 723-724-
dc.identifier.issn1554-8627-
dc.identifier.urihttp://hdl.handle.net/10722/214328-
dc.description.abstractAutophagy can dictate changes in cell metabolism via numerous mechanisms. ADIPOQ/adiponectin has been extensively characterized to have beneficial metabolic effects, both via INS/insulin-sensitizing and INS-independent actions. Our recent work examined the regulation of skeletal muscle autophagy by ADIPOQ and the functional significance. We showed that ADIPOQ directly stimulates autophagic flux in cultured skeletal muscle cells via an AMPK-dependent signaling pathway leading to phosphorylation of ULK1 (Ser555). Pharmacological inhibition of autophagy or overexpressing an inactive mutant of ATG5 to create an autophagy-deficient cell model reduces INS sensitivity. A high-fat diet (HFD) does not induce skeletal muscle autophagy in Adipoq knockout (Ad-KO) mice, whereas it does in wild-type (WT) mice, although ADIPOQ replenishment in Ad-KO mice stimulates autophagy. Changes in skeletal muscle autophagy correlate well with peripheral INS sensitivity and glucose metabolism. Thus, ADIPOQ stimulates autophagic flux in skeletal muscle, which likely represents one important mechanism mediating multiple favorable metabolic effects.-
dc.languageeng-
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/autophagy/index.php-
dc.relation.ispartofAutophagy-
dc.titleEmerging role of autophagy in mediating widespread actions of ADIPOQ/adiponectin-
dc.typeArticle-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.doi10.1080/15548627.2015.1034418-
dc.identifier.pmid25905437-
dc.identifier.pmcidPMC4502648-
dc.identifier.hkuros246873-
dc.identifier.volume11-
dc.identifier.issue4-
dc.identifier.spage723-
dc.identifier.epage724-
dc.publisher.placeUnited States-

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