A study published in Science (2009) shows that deletion of the ribosomal S6 protein kinase 1 (S6K1) in mice increases lifespan and improves age-related pathologies such as bone, immune, and motor dysfunction, and insulin resistance. The results suggest that S6K1 and AMPK signaling may be manipulated to mimic caloric restriction (CR) and provide protection against aging-related diseases. The study found that S6K1 deletion led to gene expression patterns similar to those seen in CR or AMPK activation. In female mice, S6K1 deletion significantly increased lifespan, while no effect was observed in males. Female S6K1-deficient mice showed improvements in motor function, immune function, and bone health. They also had increased insulin sensitivity and reduced adiposity. The study also found that S6K1 deletion led to changes in gene expression in the liver, skeletal muscle, and white adipose tissue that were similar to those seen in CR. These changes included increased expression of genes associated with PPAR signaling, lipid metabolism, and AMPK activity. The study also showed that in C. elegans, S6K1 deletion increased AMPK activity, which may contribute to increased lifespan. The findings suggest that manipulating S6K1 and AMPK signaling could be a potential therapeutic approach for aging-related diseases.A study published in Science (2009) shows that deletion of the ribosomal S6 protein kinase 1 (S6K1) in mice increases lifespan and improves age-related pathologies such as bone, immune, and motor dysfunction, and insulin resistance. The results suggest that S6K1 and AMPK signaling may be manipulated to mimic caloric restriction (CR) and provide protection against aging-related diseases. The study found that S6K1 deletion led to gene expression patterns similar to those seen in CR or AMPK activation. In female mice, S6K1 deletion significantly increased lifespan, while no effect was observed in males. Female S6K1-deficient mice showed improvements in motor function, immune function, and bone health. They also had increased insulin sensitivity and reduced adiposity. The study also found that S6K1 deletion led to changes in gene expression in the liver, skeletal muscle, and white adipose tissue that were similar to those seen in CR. These changes included increased expression of genes associated with PPAR signaling, lipid metabolism, and AMPK activity. The study also showed that in C. elegans, S6K1 deletion increased AMPK activity, which may contribute to increased lifespan. The findings suggest that manipulating S6K1 and AMPK signaling could be a potential therapeutic approach for aging-related diseases.