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Fermented mealworm extract prevents concurrent bone and muscle loss by modulating RANKL-NFκB/MAPK signaling in
Soo-Young Choi1, Mi-Kyung Lee1
1Department of Food and Nutrition, Sunchon National University, Suncheon, 57922, Republic of Korea.
Abstract:
This study investigated whether fermented mealworms extract (FME) can simultaneously improve postmenopausal osteoporosis and muscle atrophy, along with the underlying mechanisms. Female C57BL/6 N mice were divided into five groups: sham-operated, ovariectomized (OVX), OVX treated with two doses of FME (200 and 500 mg/kg, oral), and OVX treated with alendronate (Alen, 500 μg/kg, oral) as a positive control, for 15 weeks. FME500 significantly increased grip strength, whereas FME200 showed no significant improvement compared to the OVX group. Muscle cross-sectional area significantly increased in both FME groups compared to the OVX group. FME500 also enhanced muscle protein synthesis markers (MyoD1 and MHC) and more effectively suppressed muscle degradation markers (MuRF-1, atrogin-1, myostatin, and polyubiquitinated proteins) than FME200. In bone, both FME doses improved bone density and serum levels of RANKL and CTX-1 compared to the OVX group. FME500 more effectively downregulated RANKL, IL-6, and TNF-α expression in both bone and muscle than FME200 in OVX group. Mechanistic analyses were performed mainly in the FME500 group, which downregulated NFκB/MAPK and upregulated IGF-1-PI3K-Akt in both bone and muscle. These results indicate that FME suppresses the postmenopausal concurrent bone and muscle loss by regulating RANKL-NFκB/MAPK and IGF-1-PI3K-Akt signaling pathways.
Insights
Fermented mealworm extract (FME) shows promise in combating postmenopausal bone loss and muscle atrophy. The 500 mg/kg dose significantly improved muscle strength and bone density by regulating key signaling pathways.
Area of Science:
- Biochemistry
- Gerontology
- Nutritional Science
Background:
- Postmenopausal osteoporosis and muscle atrophy are significant health concerns.
- Concurrent bone and muscle loss negatively impacts quality of life and mobility.
- Current treatments may have limitations, necessitating novel therapeutic approaches.
Purpose of the Study:
- To investigate the efficacy of fermented mealworm extract (FME) in simultaneously improving postmenopausal osteoporosis and muscle atrophy.
- To elucidate the underlying molecular mechanisms of FME action in bone and muscle tissues.
- To compare the effects of different FME doses and alendronate in a mouse model.
Main Methods:
- Female C57BL/6N mice were ovariectomized (OVX) to mimic postmenopausal conditions.
- Groups received sham operation, OVX, OVX + FME (200 and 500 mg/kg), or OVX + alendronate for 15 weeks.
- Muscle strength (grip strength), muscle cross-sectional area, and protein markers were assessed.
- Bone mineral density, RANKL, CTX-1, IL-6, and TNF-α levels were measured.
- Signaling pathways (NFκB/MAPK, IGF-1-PI3K-Akt) were analyzed.
Main Results:
- FME at 500 mg/kg significantly increased grip strength and muscle cross-sectional area.
- Both FME doses improved bone density and modulated serum RANKL and CTX-1 levels.
- FME500 demonstrated superior suppression of muscle degradation markers (MuRF-1, atrogin-1) and inflammatory cytokines (IL-6, TNF-α).
- FME downregulated NFκB/MAPK and upregulated IGF-1-PI3K-Akt signaling in both bone and muscle tissues.
Conclusions:
- Fermented mealworm extract (FME) effectively mitigates concurrent bone loss and muscle atrophy in a postmenopausal mouse model.
- The beneficial effects are mediated through the regulation of RANKL-NFκB/MAPK and IGF-1-PI3K-Akt signaling pathways.
- FME, particularly at 500 mg/kg, represents a potential therapeutic agent for age-related musculoskeletal decline.
