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

ABSTRACT:

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-tr

SUBMITTER: Langer HT 

PROVIDER: S-EPMC11250533 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature