Restoring adiponectin via rosiglitazone ameliorates tissue wasting in mice with lung cancer
Acta Physiologica, 2024•Wiley Online Library
Aim To investigate systemic regulators of the cancer‐associated cachexia syndrome (CACS)
in a pre‐clinical model for lung cancer with the goal to identify therapeutic targets for tissue
wasting. Methods Using the Kras/Lkb1 (KL) mouse model, we found that CACS is
associated with white adipose tissue (WAT) dysfunction that directly affects skeletal muscle
homeostasis. WAT transcriptomes showed evidence of reduced adipogenesis, and, in
agreement, we found low levels of circulating adiponectin. To preserve adipogenesis and …
in a pre‐clinical model for lung cancer with the goal to identify therapeutic targets for tissue
wasting. Methods Using the Kras/Lkb1 (KL) mouse model, we found that CACS is
associated with white adipose tissue (WAT) dysfunction that directly affects skeletal muscle
homeostasis. WAT transcriptomes showed evidence of reduced adipogenesis, and, in
agreement, we found low levels of circulating adiponectin. To preserve adipogenesis and …
Aim
To investigate systemic regulators of the cancer‐associated cachexia syndrome (CACS) in a pre‐clinical model for lung cancer with the goal to identify therapeutic targets for tissue wasting.
Methods
Using the Kras/Lkb1 (KL) mouse model, we found that CACS is associated with white adipose tissue (WAT) dysfunction that directly affects skeletal muscle homeostasis. WAT transcriptomes showed evidence of reduced adipogenesis, and, in agreement, we found low levels of circulating adiponectin. To preserve adipogenesis and restore adiponectin levels, we treated mice with the PPAR‐γ agonist, rosiglitazone.
Results
Rosiglitazone treatment increased serum adiponectin levels, delayed weight loss, and preserved skeletal muscle and adipose tissue mass, as compared to vehicle‐treated mice. The preservation of muscle mass with rosiglitazone was associated with increases in AMPK and AKT activity. Similarly, activation of the adiponectin receptors in muscle cells increased AMPK activity, anabolic signaling, and protein synthesis.
Conclusion
Our data suggest that PPAR‐γ agonists may be a useful adjuvant therapy to preserve tissue mass in lung cancer.
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