Title : In vivo and in vitro evidence that chronic activation of the hexosamine biosynthetic pathway interferes with
leptin-dependent
STAT3 phosphorylation
Abstract :
- We previously reported that a 2-day peripheral infusion of glucosamine caused leptin resistance in rats, suggesting a role for the hexosamine biosynthetic pathway ( HBP ) in the development of leptin resistance
- Here we tested leptin responsiveness in mice in which HBP activity was stimulated by offering 30% sucrose solution in addition to chow and water or by infusing glucosamine
- Mice were leptin resistant after 33 days of access to sucrose
- Resistance was associated with increased activity of the HBP and with phosphorylation of transcription factor signal transducer and activator of transcription-3 Tyr705 [p STAT3 (Y705)] but inhibition of suppressor of cytokine signaling 3 in the liver and hypothalamus
- Intravenous infusion of glucosamine for 3 h stimulated p STAT3 (Y705) but prevented leptin-induced phosphorylation of STAT3 ( S727 )
- In an in vitro system, glucose, glucosamine, and leptin each dose dependently increased O-linked β-N-acetylglucosamine ( O-GlcNAc ) protein and p STAT3 (Y705) in HepG2 cells
- To test the effect of glucose on leptin responsiveness cells were incubated in 5.5 mM (LG) or 20 mM (HG) glucose for 18 h and were treated with 0 or 50 ng/ml leptin for 15 min
- HG alone and LG + leptin produced similar increases in O-GlcNAc protein, glutamine fructose-6-phosphate amidotransferase ( GFAT ), and p STAT3 (Y705) compared with LG media
- Leptin did not stimulate these proteins in HG cells, suggesting leptin resistance
- Leptin-induced p STAT3 ( S727 ) was prevented by HG media
- Inhibition of GFAT with azaserine prevented LG + leptin and HG stimulation of p STAT3
- These data demonstrate development of leptin resistance in sucrose-drinking mice and provide new evidence of leptin-induced stimulation of the HBP
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protein,
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Output(Part-Of) (sent_index,
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*Output_Site_Fusion* (sent_index,
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