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- W66016706 abstract "Adiponectin and leptin have been shown to regulate energy metabolism in skeletal muscle. However, little is known regarding their signaling crosstalk. Hyperleptinemia is a common feature in human obesity and here we investigated effects of leptin (60 nM, 24 hours) on functions of recombinant globular (gAd) and full-length multimers (fAd) of adiponectin in L6 skeletal muscle cells. Real-time PCR showed that mRNA expression levels of adiponectin receptor 1 (AdipoR1) and AdipoR2 were reduced after leptin treatment. Correspondingly, effects of both gAd and fAd on glucose and fatty acid uptake and oxidation were attenuated. AMPK is thought to be an important mediator of metabolic effects of adiponectin and here we showed that Compound C (AMPK inhibitor) pretreatment prevented stimulation of fatty acid uptake by fAd. Importantly, the activation of AMPK and ACC by gAd and fAd was attenuated by leptin. APPL1 was recently identified as an adaptor protein interacting with AdipoR and downstream targets such as Akt. Here we observed that leptin also regulated Ad-stimulated binding of APPL1 to these targets. These results suggest that hyperleptinemia can induce resistance to gAd and fAd in skeletal muscle cells, possibly due to the reduction of AdipoR expression." @default.
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- W66016706 date "2008-03-01" @default.
- W66016706 modified "2023-09-26" @default.
- W66016706 title "Hyperleptinemia induced adiponectin resistance in rat skeletal muscle cells" @default.
- W66016706 doi "https://doi.org/10.1096/fasebj.22.1_supplement.614.16" @default.
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