The Publication:

Quercetin Improved Muscle Mass and Mitochondrial Content in a Murine Model of Cancer and Chemotherapy-Induced Cachexia

Sounds like a mouthful? Don’t worry—there’s a summary below.

Publication Summary:

Cachexia, also known as wasting syndrome, is a complex metabolic condition characterized by severe weight loss, muscle atrophy, fatigue, weakness, and significant loss of appetite in someone not actively trying to lose weight. Cachexia is commonly associated with serious diseases such as cancer and cancer treatment, heart failure, chronic obstructive pulmonary disease (COPD), kidney disease, and AIDS. The exact cause of cachexia is not fully understood, but it is believed to be the result of a systemic inflammatory response. The management of cachexia can be challenging, and there are no FDA-approved drugs to ameliorate the complications of cancer cachexia. Quercetin, an organic polyphenolic flavonoid, has demonstrated anti-inflammatory and antioxidant properties with promise in protecting against cancer and chemotherapy-induced dysfunction; however, whether quercetin is efficacious in maintaining muscle mass in tumor-bearing animals receiving chemotherapy has not been investigated.  Mice bearing a type of colon tumor (C26) were given chemotherapy drug 5-fluorouracil (5FU, 30 mg/kg of lean mass) concomitant with quercetin (Quer; 50 mg/kg of body weight) or vehicle. Both C26 + 5FU mice and C26 + 5FU + Quer mice had similar body weight loss; however, muscle mass and cross-sectional area was greater in C26 + 5FU + Quer mice compared to C26 + 5FU mice. Additionally, C26 + 5FU + Quer mice had a greater number and larger intermyofibrillar mitochondria with increased relative protein expression of mitochondrial complexes V, III, and II as well as cytochrome c expression. C26 + 5FU + Quer mice also had increased MFN1 and reduced FIS1 relative protein expression without apparent benefits to muscle inflammatory signaling. Our data suggest that quercetin protected against cancer and chemotherapy-induced muscle mass loss through improving mitochondrial homeostatic balance.