Flurbiprofen ameliorates glucose deprivation-induced leptin resistance

• Main Authors: Toru Hosoi (Author), Yuka Suyama (Author), Takaaki Kayano (Author), Koichiro Ozawa (Author)
• Format: Book
• Published: Frontiers Media S.A., 2016-09-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 1663-9812; 10.3389/fphar.2016.00354
• Keywords: Glucose; Leptin; Neuron; Stat5; AMPK; stat3; Therapeutics. Pharmacology; RM1-950
• Source: Frontiers in Pharmacology, Vol 7 (2016)

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.