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ORIGINAL ARTICLE
Year : 2021  |  Volume : 64  |  Issue : 5  |  Page : 211-217

Mealworm (Tenebrio molitor)-derived protein supplementation attenuates skeletal muscle atrophy in hindlimb casting immobilized rats


1 Department of Physiology, College of Medicine, Soonchunhyang University, Cheonan, Korea
2 Department of Sports Science, Institute of Sports Health Science, Sunmoon University, Asan, South Korea

Correspondence Address:
Dr. Young-Ju Song
Institute of Sports Health Science, Sunmoon University, Asan 31460
South Korea
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cjp.cjp_40_21

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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 mealworm-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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