Digital Repository

Pterostilbene reverses palmitic acid mediated insulin resistance in HepG2 cells by reducing oxidative stress and triglyceride accumulation

Show simple item record Ahmad Malik, Sajad en_US Acharya, Jhankar en_US MEHENDALE, NEELAY en_US KAMAT, SIDDHESH S. en_US Ghaskadbi, Saroj S. en_US 2019-06-26T04:00:26Z 2019-06-26T04:00:26Z 2019-07 en_US
dc.identifier.citation Free Radical Research, 53(7). en_US
dc.identifier.issn 1071-5762 en_US
dc.identifier.issn 1029-2470 en_US
dc.identifier.uri en_US
dc.description.abstract Insulin resistance (IR) is known to precede onset of type 2 diabetes and increased oxidative stress appears to be a deleterious factor leading to IR. In this study, we evaluated ability of pterostilbene (PTS), a methoxylated analogue of resveratrol and a known antioxidant, to reverse palmitic acid (PA)-mediated IR in HepG2 cells. PTS prevented reactive oxygen species (ROS) formation and subsequent oxidative lipid damage by reducing the expression of NADPH oxidase 3 (NOX3) in PA treated HepG2 cells. Hepatic glucose production was used as a measure of IR and PTS reversed PA-mediated increase in hepatic glucose production by reducing expression of genes coding for gluconeogenic enzymes namely glucose-6-phosphatase (G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and pyruvate carboxylase (PC); and their transcription factors cAMP response element binding protein (CREB) and fork head class Box O (FOXO1) along with its coactivator peroxisome proliferator-activated receptor gamma co-activator-1 α (PGC1α). PTS reversed PA-mediated activation of c-Jun N-terminal kinase (JNK), which in turn altered insulin signalling pathway by phosphorylating IRS-1 at Ser 307, leading to inhibition of phosphorylation of Akt and GSK-3β. PTS also reduced PA-mediated lipid accumulation by reducing expression of transcription factors SREBP1c and PPARα. SREBP1c activates genes involved in fatty acid and triglyceride synthesis while PPARα activates CPT1, a rate limiting enzyme for controlling entry and oxidation of fatty acids into mitochondria. PTS, however, did not influence PA uptake confirmed by using BODIPY-labelled fluorescent C16 fatty acid analogue. Thus, our data provides a possible mechanistic explanation for reversal of PA-mediated IR in HepG2 cells. en_US
dc.language.iso en en_US
dc.publisher Taylor & Francis en_US
dc.subject Gluconeogenesis en_US
dc.subject Insulin resistance en_US
dc.subject Oxidative stress en_US
dc.subject Palmitic acid en_US
dc.subject Pterostilbene en_US
dc.subject Reactive oxygen species en_US
dc.subject TOC-JUN-2019 en_US
dc.subject 2019 en_US
dc.title Pterostilbene reverses palmitic acid mediated insulin resistance in HepG2 cells by reducing oxidative stress and triglyceride accumulation en_US
dc.type Article en_US
dc.contributor.department Dept. of Biology en_US
dc.identifier.sourcetitle Free Radical Research en_US
dc.publication.originofpublisher Foreign en_US

Files in this item

Files Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record

Search Repository

Advanced Search


My Account