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Understanding the tissue-specific role of insulin signalling reduction on mammalian lifespan and health
Understanding the tissue-specific role of insulin signalling reduction on mammalian lifespan and health
Reduced insulin/insulin-like growth factor signaling (IIS) extends health and lifespan in mammals. Loss of IRS1 increases survival in mice, but the tissues responsible for this effect are unknown. Tissue-specific loss of IRS1 did not increase survival, but lack of IRS1 in more than one tissue is required for lifespan extension. Loss of IRS1 in liver, muscle, and fat did not improve health. However, loss of neuronal IRS1 increased energy expenditure, locomotion, and insulin sensitivity in old male mice. Therefore, this brain signature of aging in response to reduced IIS was associated with improved health at old age in male mice.
Increased lifespan and healthspan in mice lacking IRS1
Increased lifespan and healthspan in mice lacking IRS1
Tissue-specific knockout of IRS1 in liver, muscle, fat or neurons does not extend lifespan in mice
Tissue-specific knockout of IRS1 in liver, muscle, fat or neurons does not extend lifespan in mice
Neuron-specific deletion of Irs1 causes male-specific benefits to metabolic health
Neuron-specific deletion of Irs1 causes male-specific benefits to metabolic health
Loss of IRS1 function led to mitochondrial dysfunction, activation of the ISR and cellular metabolic adaptations in the brains of old male mice
Loss of IRS1 function led to mitochondrial dysfunction, activation of the ISR and cellular metabolic adaptations in the brains of old male mice
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