Abstract
Honeybees produce royal jelly (RJ) from their cephalic glands. Royal jelly is a source of nutrition for the queen honey bee throughout its lifespan and is also involved in fertility and longevity. Royal jelly has long been considered beneficial to human health. We recently observed that RJ delayed impairment of motor function during aging, affecting muscle fiber size. However, how RJ affects skeletal muscle metabolism and the functional component of RJ is as of yet unidentified. We demonstrate that feeding mice with RJ daily prevents a decrease in myofiber size following denervation without affecting total muscle weight. RJ did not affect atrophy-related genes but stimulated the expression of myogenesis-related genes, including IGF-1 and IGF receptor. Trans-10-hydroxy-2-decenoic acid (10H2DA) and 10-hydroxydecanoic acid (10HDAA), two major fatty acids contained in RJ. After ingestion, 10H2DA and 10HDAA are metabolized into 2-decenedioic acid (2DA) and sebacic acid (SA) respectively. We found that 10H2DA, 10HDAA, 2DA, and SA all regulated myogenesis of C2C12 cells, murine myoblast cells. These novel findings may be useful for potential preventative and therapeutic applications for muscle atrophy disease included in Sarcopenia, an age-related decline in skeletal muscle mass and strength.
Highlights
Sarcopenia is an age-related decline in skeletal muscle mass and strength [1]
We demonstrate that feeding mice daily with protease-treated royal jelly (pRJ) prevents a decrease in myofiber size following denervation
We showed that pRJ affects muscle fiber size in elderly mice without changing total muscle weight [35]
Summary
Sarcopenia is an age-related decline in skeletal muscle mass and strength [1]. Muscle fiber degeneration and impaired satellite cell regeneration contribute to Sarcopenia. Major royal jelly protein 1(MRJP) is a frequent allergen for honey-related allergies [30]. To eliminate such adverse events with RJ supplementation, protease-treated RJ (pRJ) has been developed by treating RJ with alkaline proteases, leading to complete elimination of MRJP without nutritional loss of minerals, vitamins, and fatty acids [31]. In mice, feeding of RJ increases the serum IGF1 levels and stimulates regeneration of injured muscle via the IGF1-Akt pathway in satellite cells [32]. Treatment of C2C12 myoblasts with pRJ and pRJ-related fatty acids stimulated differentiation and proliferation
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