Inducing Low Body Temperature via Torpor Slows Aging in Mice
Past evidence has suggested that the lowered body temperature characteristic of calorie restriction is important to the slowed aging that results in short-lived mammals. One might compare that to the strong evidence for upregulated autophagy to be the driving factor in slowed aging produced by the practice of calorie restriction. Researchers here conduct a similar study, inducing a reduction in metabolic rate, dietary intake, and body temperature in mice via activation of a specific brain region. As in past research, the resulting slowed aging was shown to be driven by that lowered body temperature rather than any of the other effects of this intervention.
Torpor and hibernation are extreme physiological adaptations of homeotherms associated with pro-longevity effects. Yet the underlying mechanisms of how torpor affects aging, and whether hypothermic and hypometabolic states can be induced to slow aging and increase health span, remain unknown. We demonstrate that the activity of a spatially defined neuronal population in the anterior and ventral portions of the medial and lateral preoptic area (avMLPA), which has previously been identified as a torpor-regulating brain region, is sufficient to induce a torpor like state (TLS) in mice.
Prolonged induction of TLS slows epigenetic aging across multiple tissues and improves health span. We isolate the effects of decreased metabolic rate, long-term caloric restriction, and decreased core body temperature (Tb) on blood epigenetic aging and find that the pro-longevity effect of torpor-like states is mediated by decreased Tb. Taken together, our findings provide novel mechanistic insight into the pro-longevity effects of torpor and hibernation and support the growing body of evidence that Tb is an important mediator of aging processes.