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Early study initially suggested that disruptions of the insulin or GH/IGF1 axis with low insulin and IGF1 levels may enhance autophagy to prevent the age-related mitochondrial degradation and extend the lifespan (Wang and Miller (2012) demonstrated that fibroblasts in Snell mice (which secrete very low amounts of GH, prolactin, and thyroid-stimulating hormone) are more susceptible to autophagy induced by amino acid withdrawal or by oxidative stress than control cells

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