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Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.
Specimen part
View SamplesWith the population of older and overweight individuals on the rise in the Western world, there is an ever greater need to slow the aging processes and reduce the burden of age-associated chronic disease that would significantly improve the quality of human life and reduce economic costs. Caloric restriction (CR), is the most robust and reproducible intervention known to delay aging and to improve healthspan and lifespan across species (1); however, whether this intervention can extend lifespan in humans is still unknown. Here we report that rats and humans exhibit similar responses to long-term CR at both the physiological and molecular levels. CR induced broad phenotypic similarities in both species such as reduced body weight, reduced fat mass and increased the ratio of muscle to fat. Likewise, CR evoked similar species-independent responses in the transcriptional profiles of skeletal muscle. This common signature consisted of three key pathways typically associated with improved health and survival: IGF-1/insulin signaling, mitochondrial biogenesis and inflammation. To our knowledge, these are the first results to demonstrate that long-term CR induces a similar transcriptional profile in two very divergent species, suggesting that such similarities may also translate to lifespan-extending effects in humans as is known to occur in rodents. These findings provide insight into the shared molecular mechanisms elicited by CR and highlight promising pathways for therapeutic targets to combat age-related diseases and promote longevity in humans.
Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.
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View SamplesWe constructed a polycistronic lentiviral vector to overexpress 3 germ cell specific genes (Stella, Oct4 and Nanos2) in mouse embryonic fibroblast (MEFs) and evaluated the transcriptome portrait in partially reprogrammed cells.We sequenced RNA samples from bulk cell population of two biological duplicates of MEF-GFP (control) and MEF-SON (overexpressed) 21 days post infection. Differential expression analysis of 50 M pair-end read per samples showed overexpression of neurogenesis, blood vessel and proliferation related genes and downregulation of chondroitin sulphate metabolic process, nitric oxide production and innate immune response genes. Overall design: Examination of whole transcriptome following concurrent overexpression of Stella, Oct4 and Nanos2 in MEFs.
Suppression of dsRNA response genes and innate immunity following Oct4, Stella, and Nanos2 overexpression in mouse embryonic fibroblasts.
Specimen part, Cell line, Subject
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