Mealworm (Tenebrio molitor)-Derived Protein Supplementation Attenuates Skeletal Muscle Atrophy in Hindlimb Casting Immobilized Ratsopen access
- Authors
- Lee, Jeong-Beom; Kwon, Dae-Keun; Jeon, Yoo-Jeong; Song, Young-Ju
- Issue Date
- Sep-2021
- Publisher
- Chinese Physiology Society/Chung-kuo Sheng Li Hsueh Hui
- Keywords
- Hindlimb casted immobilized rat; immobilization; mealworm; muscle atrophy; sarcopenia
- Citation
- Chinese Journal of Physiology, v.64, no.5, pp 211 - 217
- Pages
- 7
- Journal Title
- Chinese Journal of Physiology
- Volume
- 64
- Number
- 5
- Start Page
- 211
- End Page
- 217
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/20776
- DOI
- 10.4103/cjp.cjp_40_21
- ISSN
- 0304-4920
2666-0059
- Abstract
- This study aimed to investigate the effect of mealworm (Tenebrio molitor) derived protein supplementation on skeletal muscle atrophy of hindlimb casted immobilized rats. Twenty-four six-week-old male Sprague-Dawley rats were randomly divided into three groups: control sedentary group (CD, n = 8), control diet casting group (CDC, n = 8), and the mealworm-derived protein supplemented casting group (MDC, n = 8). CD and CDC group was supplemented AIN-76G diet and mealwonn-derived protein supplemented diet for MDC group was substituted as 5% casein protein to 5% mealworm protein for 5 weeks and left hindlimb casting immobilization using casting tape for CDC and MDC group was done 1 week before sacrifice. After 5 weeks of mealworm supplementation, the soleus muscle weight of the MDC group was significantly higher compared to the CDC group. In addition, the level of muscle protein synthesis factors p-Akt/Akt, p-4EBP1/4EBP1, and p-S6K/S6K significantly increased in the MDC group compared to the CDC group. On contrary, the level of muscle protein degradation factors (MuRF1 and atrogin-1) was significantly lower in the MDC group than that of the CDC group. These results suggest that mealworm-derived protein supplementation may have a significant role in the prevention of skeletal muscle atrophy via stimulation of muscle protein synthesis factors and inhibition of muscle protein degradation factors, and therefore a promising intervention in sarcopenia.
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