Flurbiprofen ameliorates glucose deprivation-induced leptin resistance
Leptin resistance is one of the mechanisms involved in the pathophysiology of obesity. The present study showed that glucose deprivation inhibited leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) and signal transducer and activator of transcription 5 (STAT...
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| Main Authors: | , , , |
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| Format: | Book |
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Frontiers Media S.A.,
2016-09-01T00:00:00Z.
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| Summary: | Leptin resistance is one of the mechanisms involved in the pathophysiology of obesity. The present study showed that glucose deprivation inhibited leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) and signal transducer and activator of transcription 5 (STAT5) in neuronal cells. Flurbiprofen reversed glucose deprivation-mediated attenuation of STAT3, but not STAT5 activation, in leptin-treated cells. Glucose deprivation increased C/EBP-homologous protein (CHOP) and glucose regulated protein 78 (GRP78) induction, indicating the activation of unfolded protein responses (UPR). Flurbiprofen did not affect the glucose deprivation-induced activation of UPR, but did attenuate the glucose deprivation-mediated induction of AMP-activated protein kinase (AMPK) phosphorylation. Flurbiprofen may ameliorate glucose deprivation-induced leptin resistance in neuronal cells. |
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| Item Description: | 1663-9812 10.3389/fphar.2016.00354 |