Reduction of the number and functional capacity of the muscle satellite cells is considered a core contributor to the development of age-related muscular dysfunction [96]. Induction of myogenesis via in vivo reprogramming of muscle satellite cells is a currently studied strategy that has not been successfully used for sarcopenia treatment yet [143]. On the other hand, treating sarcopenic rats with both royal jelly and pRJ was reported to increase the number of Pax7-positive satellite cells in vivo and in vitro (pRJ only). pRJ induced self-renewal of satellite cells via activation of AKT signaling [96,97]. AKT activity was associated with activation of IGF-1 as indicated by increased serum levels of IGF-1. IGF-1 plays a crucial rule in the activation of various signaling pathways; it is believed to be a major mediator of muscle growth and repair that functions by stimulating the proliferation and differentiation of satellite cells into myotubes, albeit the exact mechanism is not clear yet [96]. Similarly, pRJ activated AKT-signaling pathway in satellite cells culture, which was associated with increased proliferation of myosatellite cells and their differentiation into myotubes—an effect that is contradictory to muscle loss. AKT is thought to contribute to the synthesis of muscular proteins and inhibition of muscle proteolysis [96].