File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Fenofibrate insulates diacylglycerol in lipid droplet/ER and preserves insulin signaling transduction in the liver of high fat fed mice

TitleFenofibrate insulates diacylglycerol in lipid droplet/ER and preserves insulin signaling transduction in the liver of high fat fed mice
Authors
Issue Date2015
Citation
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2015, v. 1852 n. 7, p. 1511-1519 How to Cite?
AbstractHepatic steatosis is often associated with insulin resistance as a hallmark of the metabolic syndrome in the liver. The present study investigated the effects of PPARα activation induced by fenofibrate (FB) on the relationship of insulin resistance and hepatic steatosis in mice fed a high-fat (HF) diet, which increases lipid influx into the liver. Mice were fed HF diet to induce insulin resistance and hepatic steatosis with or without FB. FB activated PPARα and ameliorated HF diet-induced glucose intolerance and hepatic insulin resistance without altering either hepatic steatosis or inflammation signaling (JNK or IKK). Interestingly, FB treatment simultaneously increased fatty acid (FA) synthesis (50%) and oxidation (66%, both p<0.01) into intermediate lipid metabolites, suggesting a FA oxidation-synthesis cycling in operation. Associated with these effects, diacylglycerols (DAGs) were sequestered within the lipid droplet/ER compartment, thus reducing their deposition in the cellular membrane, which is known to impair insulin signal transduction. These findings suggest that the reduction in membrane DAGs (rather than total hepatic steatosis) may be critical for the protection by fenofibrate-induced PPARα activation against hepatic insulin resistance induced by dietary fat
Persistent Identifierhttp://hdl.handle.net/10722/214324

 

DC FieldValueLanguage
dc.contributor.authorChan, SMH-
dc.contributor.authorZeng, XY-
dc.contributor.authorSun, RQ-
dc.contributor.authorJo, E-
dc.contributor.authorZhou, X-
dc.contributor.authorWang, H-
dc.contributor.authorLi, S-
dc.contributor.authorXu, A-
dc.contributor.authorWatt, MJ-
dc.contributor.authorYe, JM-
dc.date.accessioned2015-08-21T11:14:26Z-
dc.date.available2015-08-21T11:14:26Z-
dc.date.issued2015-
dc.identifier.citationBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2015, v. 1852 n. 7, p. 1511-1519-
dc.identifier.urihttp://hdl.handle.net/10722/214324-
dc.description.abstractHepatic steatosis is often associated with insulin resistance as a hallmark of the metabolic syndrome in the liver. The present study investigated the effects of PPARα activation induced by fenofibrate (FB) on the relationship of insulin resistance and hepatic steatosis in mice fed a high-fat (HF) diet, which increases lipid influx into the liver. Mice were fed HF diet to induce insulin resistance and hepatic steatosis with or without FB. FB activated PPARα and ameliorated HF diet-induced glucose intolerance and hepatic insulin resistance without altering either hepatic steatosis or inflammation signaling (JNK or IKK). Interestingly, FB treatment simultaneously increased fatty acid (FA) synthesis (50%) and oxidation (66%, both p<0.01) into intermediate lipid metabolites, suggesting a FA oxidation-synthesis cycling in operation. Associated with these effects, diacylglycerols (DAGs) were sequestered within the lipid droplet/ER compartment, thus reducing their deposition in the cellular membrane, which is known to impair insulin signal transduction. These findings suggest that the reduction in membrane DAGs (rather than total hepatic steatosis) may be critical for the protection by fenofibrate-induced PPARα activation against hepatic insulin resistance induced by dietary fat-
dc.languageeng-
dc.relation.ispartofBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease-
dc.titleFenofibrate insulates diacylglycerol in lipid droplet/ER and preserves insulin signaling transduction in the liver of high fat fed mice-
dc.typeArticle-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.doi10.1016/j.bbadis.2015.04.005-
dc.identifier.hkuros246868-
dc.identifier.volume1852-
dc.identifier.issue7-
dc.identifier.spage1511-
dc.identifier.epage1519-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats