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Restoring adiponectin via rosiglitazone ameliorates tissue wasting in mice with lung cancer.

Henning Tim LangerShakti RamsamoojEzequiel DantasAnirudh MurthyMujmmail AhmedSeo-Kyoung HwangRahul GroverRita PozovskiyRoger J LiangAndre Lima QueirozJustin C BrownEileen P WhiteTobias JanowitzMarcus D Goncalves
Published in: bioRxiv : the preprint server for biology (2023)
- The PPAR-γ agonist, rosiglitazone, restores circulating adiponectin levels in mice with lung cancer.- Rosiglitazone preserves skeletal muscle and adipose tissue mass in mice with lung cancer.- The preservation of muscle mass with rosiglitazone is associated with increases in AMPK and AKT activity.- Stimulation of adiponectin signaling increases AMPK activity, anabolic signaling, and protein synthesis in muscle cell culture.
Keyphrases
  • insulin resistance
  • skeletal muscle
  • high fat diet induced
  • adipose tissue
  • metabolic syndrome
  • high fat diet
  • cell proliferation
  • signaling pathway
  • mouse model