Results indicate that T. borchii extracts can attenuate selected cellular alterations associated with muscle aging, and future identification of the most active components may support their development as nutraceutical supplements.
Abstract
Background/Objectives: Sarcopenia involves a gradual decline in skeletal muscle mass that may occur during aging or in association with chronic pathological conditions. It markedly reduces muscle strength and mobility, thereby impairing quality of life. Because sarcopenia’s severity directly correlates with frailty, it represents an important predictor of prognosis and disease risk. Current preventive and therapeutic strategies rely mainly on physical activity, which is not feasible for all patients. This study investigated the biological effects of two independently prepared Tuber borchii (T. borchii) extracts in an in vitro model of sarcopenic stress. Methods: The activity of T. borchii extracts was investigated in a cell-based model of sarcopenia, following previous observations that these preparations influence proliferation-related pathways, including ERK1/2 phosphorylation. Specifically, differentiated myotubes were exposed to D-galactose to reproduce atrophy-associated cellular changes, and the impact of T. borchii extracts on protein synthesis, turnover, and cell morphology was assessed. Results: T. borchii extracts enhanced protein synthesis and turnover in myotubes. Furthermore, the treatment significantly reduced the expression of key galactose-induced sarcopenia and atrophy markers, such as MuRF1. Morphological analysis confirmed this protective effect, showing that treated myotubes maintained greater thickness and exhibited a larger cross-sectional area despite exposure to the sarcopenic stimulus. Conclusions: These results indicate that T. borchii extracts can attenuate selected cellular alterations associated with muscle aging. Future identification of the most active components may support their development as nutraceutical supplements.
Muscles are essential for moving and protecting the body from an external impact. However, when muscle mass decreases due to aging, lack of exercise, or nutritional deficiency, muscle atrophy occurs. Persistent muscle atrophy leads to physical limitations, fatigue, and serious health issues, ultimately decreasing the...
Hye-Jeong Hwang, Mina Kim, Kyung-A Hwang· ACS Nutrition Science· 0 citations
Introduction Skeletal muscles are crucial for voluntary movement, posture, breathing, joint stability, and therefore are essential for maintaining overall health and quality of life. Aging, sarcopenia, cancer, immobilization, and several muscle pathologies can have an impact on muscle function, and muscle cell senescen...
K. M. Bagri, Morgana Teixeira Lima Castelo-Branco, C. Mermelstein· Frontiers in Aging· 0 citations
It is demonstrated that CSE alleviates skeletal muscle deterioration in both obesity- and aging-associated sarcopenia by reducing intramuscular lipid accumulation and improving mitochondrial metabolism, inflammatory responses, and muscle protein turnover.
Su-Kyung Shin, Jiwon Jeong, Min-Jeong Kim et al.· Frontiers in Nutrition· 0 citations
BACKGROUND & AIMS
Metabolic dysfunction-associated steatohepatitis (MASH) is frequently complicated by sarcopenia, in which mitochondrial dysfunction and inflammatory catabolic signaling are implicated. We investigated whether imeglimin, an antidiabetic mitochondrial modulator, attenuates MASH-associated muscle atrophy...
Yui Osaki, K. Kaji, N. Nishimura et al.· Biochimica et Biophysica Act...· 0 citations
Background Cachexia is a multifactorial syndrome frequently observed in cancer patients, characterized by progressive weight loss, muscle atrophy, and systemic inflammation. We recently demonstrated that supplementation with FuFA-F2, a naturally occurring lipid found in various foods, increases muscle mass in different...
Anaïs Deglos, Jennifer Falconi, Charles Géminard et al.· bioRxiv· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.