It's been shellfish every other day of late, but today we'll cast our eyes on another portion of the study of comparative longevity and differing metabolism between species. Birds and bats are both interesting for what they tell us about how metabolic processes determine species longevity:
Bats and birds live substantially longer on average than non-flying mammals of similar body size. The combination of small body size, high metabolic rates, and long lifespan in bats and birds would not seem to support oxidative theories of ageing that view senescence as the gradual accumulation of damage from metabolic byproducts. However, large-scale comparative analyses and laboratory studies on a few emerging model species have identified multiple mechanisms for resisting oxidative damage to mitochondrial DNA and cellular structures in both bats and birds.
New techniques for determining the age of free-living, wild individuals, and robustly-supported molecular phylogenies, are under development and will improve the efforts of comparative biologists to identify ecological and evolutionary factors promoting long lifespan. In the laboratory, greater development of emerging laboratory models and comparative functional genomic approaches will be needed to identify the molecular pathways of longevity extension in birds and bats.
You can also see this sort of biochemical and life expectancy difference in naked mole rats versus other rodents. In the mole-rat case, unlike bats, older animals have a great deal of oxidative damage, but don't seem to be particularly affected by it. That tells us that there are at least a couple of different ways in which the average mammal's metabolism might be made better with respect to oxidative damage - in the sense of being engineered for longer life.
What is learned from bats and naked mole-rats will no doubt be a quite different set of optimizations to those associated with calorie restriction, insulin metabolism, p53 and telomerase, or any of the other longevity mutations and changes demonstrated in recent years. Hypothetically, one could imagine a mouse breed engineered to possess all of these mutations and engineered changes in parallel - and I suspect it won't be too many more years before a research group undertakes that project in earnest.
Still, will this be relevant to those of us reading this today? I suspect not. Upgrading human metabolism is a 2030s project, and something that will plausibly only slow aging. Not so great for those of us who will be pushing 60, 70, or more by then. The best development programs are those that focus on repair rather than enhancement: fix the damage rather than changing the mechanisms to cause less damage. It is repair that is the path to rejuvenation, or reversing the progression of aging in our cells, tissues, and organs.
Sadly, repair is not the primary focus of the aging research community. Most of the pro-longevity researchers are firmly in favor of metabolic engineering to slow aging, and largely focused on the use of drugs to achieve that goal.