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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/11626
Title: Grape powder extract attenuates tumor necrosis factor α-mediated inflammation and insulin resistance in primary cultures of human adipocytes
Authors: Chia Chi Chuang
Akkarach Bumrungpert
Arion Kennedy
Angel Overman
Tiffany West
Brent Dawson
Michael K. McIntosh
The University of North Carolina at Greensboro
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine;Nursing
Issue Date: 1-Jan-2011
Citation: Journal of Nutritional Biochemistry. Vol.22, No.1 (2011), 89-94
Abstract: Grapes are rich in phenolic phytochemicals that possess anti-oxidant and anti-inflammatory properties. However, the ability of grape powder extract (GPE) to prevent inflammation and insulin resistance in human adipocytes caused by tumor necrosis factor α (TNFα), a cytokine elevated in plasma and white adipose tissue (WAT) of obese, diabetic individuals, is unknown. Therefore, we examined the effects of GPE on markers of inflammation and insulin resistance in primary cultures of newly differentiated human adipocytes treated with TNFα We found that GPE attenuated TNFα-induced expression of inflammatory genes including interleukin (IL )-6, IL-1β, IL-8, monocyte chemoattractant protein (MCP)-1, cyclooxygenase (COX)-2 and Toll-like receptor (TLR)-2. GPE attenuated TNFα-mediated activation of extracellular signal-related kinase (ERK) and c-Jun NH 2 -terminal kinase (JNK) and activator protein-1 (AP-1, i.e., c-Jun). GPE also attenuated TNFα-mediated IκBβ degradation and nuclear factor-kappa B (NF-κB) activity. Finally, GPE prevented TNFα-induced expression of protein tyrosine phosphatase (PTP)-1B and phosphorylation of serine residue 307 of insulin receptor substrate-1 (IRS-1), which are negative regulators of insulin sensitivity, and suppression of insulin-stimulated glucose uptake. Taken together, these data demonstrate that GPE attenuates TNFα-mediated inflammation and insulin resistance in human adipocytes, possibly by suppressing the activation of ERK, JNK, c-Jun and NF-κB. © 2011 Elsevier Inc.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=78649916463&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/11626
ISSN: 09552863
Appears in Collections:Scopus 2011-2015

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