ArticleActa physiologica (Oxford, England)2024
Restoring adiponectin via rosiglitazone ameliorates tissue wasting in mice with lung cancer.
Article in Acta physiologica (Oxford, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Impaired Adipose Anabolism in Pancreatic Cancer Cachexia Is Reversed by HuR Inhibition.Journal of cachexia, sarcopenia and muscle · 2026Article
- The effects of tissue inflammation on cancer cachexia.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- The RNA-binding protein HuR impairs adipose tissue anabolism in pancreatic cancer cachexia.bioRxiv : the preprint server for biology · 2025Article
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- The role of PPARγ in cancer cachexia: friend or foe?Frontiers in endocrinology · 2025Review
- Mitochondrial Quality Control: A New Perspective in Skeletal Muscle Dysfunction of Chronic Obstructive Pulmonary Disease.Aging and disease · 2024Review
- SUN1 inhibits osteogenesis and promotes adipogenesis of human adipose-derived stem cells by regulating α-tubulin and CD36 expression.Journal of cellular and molecular medicine · 2024Article
- Defining and Addressing Research Priorities in Cancer Cachexia through Transdisciplinary Collaboration.Cancers · 2024Review
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15 authors.
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Abstract
aimTo 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.
methodsUsing 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.
resultsRosiglitazone 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.
conclusionOur data suggest that PPAR-γ agonists may be a useful adjuvant therapy to preserve tissue mass in lung cancer.
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