Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 233, Issue 3, Pages 2426-2433Publisher
WILEY
DOI: 10.1002/jcp.26115
Keywords
AMPK; EPA; GPR120; SGLT1; TNF-alpha
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Funding
- Ministry of Economy and Competitivity (MINECO) of the Government of Spain [BFU2012-36089]
- CIBER Physiopathology of Obesity and Nutrition (CIBERobn), Carlos III Health Research Institute [CB12/03/30002]
- Dept. of Health, Navarra Government [67-2015]
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The aim of the present work was to investigate in Caco-2 cells whether eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid, could block the inhibitory effect of tumor necrosis factor-alpha (TNF-alpha) on sugar transport, and identify the intracellular signaling pathways involved. After pre-incubation of the Caco-2 cells with TNF-alpha and EPA for 1 hr, EPA prevented the inhibitory effect of the cytokine on alpha-methyl-D-glucose (alpha MG) uptake (15 min) and on SGLT1 expression at the brush border membrane, measured by Western blot. The ERK1/2 inhibitor PD98059 and the AMPK activator AICAR also prevented the inhibitory effect of TNF-alpha on both alpha MG uptake and SGLT1 expression. Interestingly, the AMPK inhibitor, Compound C, abolished the ability of EPA to prevent TNF-alpha-induced reduction of sugar uptake and transporter expression. The GPR120 antagonist, AH7614, also blocked the preventive effect of EPA on TNF-alpha-induced decrease of alpha MG uptake and AMPK phosphorylation. In summary, TNF-alpha inhibits alpha MG uptake by decreasing SGLT1 expression in the brush border membrane through the activation of ERK1/2 pathway. EPA prevents the inhibitory effect of TNF-alpha through the involvement of GPR120 and AMPK activation.
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