Over the years a great many studies have been conducted using laboratory animals with the aim of recording changes in life span that result from drugs, genetic alterations, and environmental conditions. The shorter-lived and less costly to maintain the species, the more studies there are - probably thousands for nematode worms, for example.

If you feel like browsing through the stacks to gain an impression of the work that has taken place over the past few decades, allow me to point you to the Lifespan Observations Database, which "collects published lifespan data across multiple species." It isn't a complete reference, but contains thousands of entries. Here are counts by species:

• C. elegans: 3315
• S. cerevisiae: 1046
• D. melanogaster: 298
• M. musculus: 175
• P. anserina: 22
• R. norvegicus: 15
• S. pombe: 12
• C. albicans: 6
• N. furzeri: 6
• E. coli: 4
• C. remanei: 2
• M. auratus: 2
• L. longipalpis: 2
• H. sapiens: 2
• E. postfasciatus: 2
• D. pseudoobscura: 1
• C. capitata: 1

Browsing the entries shows change in life span and other items of interest. For example, picking one at random for mice:

Species: Mus musculus

Strain: 129 SvEv

Lifespan: 815 days

Reference Lifespan: 761 days

Lifespan Change: 7.1%

Lifespan Measure: median

Lifespan Effect: increased

Significance: significant

Citation: Migliaccio E, Giorgio M, Mele S, Pelicci G, Reboldi P, Pandolfi PP, Lanfrancone L, Pelicci PG. (1999). The p66shc adaptor protein controls oxidative stress response and life span in mammals.. Nature 402: 309-13. [pubmed]

Details: Mice mutant for p66shc have increased life span of 30%. Homozygous mutants are longer-lived than heterozygotes.

Other phenotypes: p66shc -/- cells are more resistant to apoptosis induced by hydrogen peroxide and UV light. p66shc -/- mice are more resistant to oxidative stress induced by paraquat,

You might compare this with some of the other online databases that have been mentioned here in the past, and are interesting to look through:

• The AnAge Database
• A Comparative Cellular and Molecular Biology of Longevity Database
• A Database of Genes Related to Calorie Restriction

Source:
http://www.fightaging.org/archives/2012/11/the-lifespan-observations-database.php

Mitochondria and the damage they accumulate as a result of their operation are important in the process of degenerative aging. Further, declining mitochondrial function is a feature in many age-related conditions. Many researchers focus their studies on mitochondrial function, differences in mitochondria between species and how that determines life span, alterations in mitochondrial operation that occur in connection with life-extending interventions in laboratory animals, and similar areas. These days that often involves producing a great deal of data for later analysis:

In efforts to understand what influences life span, cancer and aging, scientists are building roadmaps to navigate and learn about cells at the molecular level. To survey previously uncharted territory, a team of [researchers] created an "atlas" that maps more than 1,500 unique landmarks within mitochondria that could provide clues to the metabolic connections between caloric restriction and aging.

The map, as well as the techniques used to create it, could lead to a better understanding of how cell metabolism is re-wired in some cancers, age-related diseases and metabolic conditions such as diabetes. "It's really a dynamic atlas for regulatory points in mitochondrial function - there are many interesting avenues that other scientists can follow up on. It could take years for researchers to understand what it all means, but at least now we have a list of the most important players."

[The scientists] conducted earlier research on the mitochondrial protein Sirt3, where they suggested a link between Sirt3 and the benefits of caloric restriction in situations such as the prevention of age-related hearing loss. The new research [more] broadly identifies pathways in mitochondria that could be behind the rewiring of metabolism. Their work uncovered regulatory processes that maintain mitochondrial health, control cells' ability to metabolize fat and amino acids, as well as stimulate antioxidant responses.

Link: http://www.news.wisc.edu/21305

Source:
http://www.fightaging.org/archives/2012/11/a-protein-map-for-mitochondrial-function.php

Lobsters are one of the small number of species that might be ageless, or at the very least age very slowly and exhibit little to no decline until very late life. There is little money for aging research in lobsters, however: until now researchers possessed no way to accurately determine the age of a lobster, and no good estimate as to average or maximum life span in these species. This new development should hopefully lead to a better grasp of the degree to which lobsters do or do not age, and pin down numbers for life span:

For the first time, scientists have figured out how to determine the age of a lobster - by counting its rings, like a tree. Nobody knows how old lobsters can live to be; some people estimate they live to more than 100.

Scientists already could tell a fish's age by counting the growth rings found in a bony part of its inner ear, a shark's age from the rings in its vertebrae and a scallop or clam's age from the rings of its shell. But crustaceans posed a problem because of the apparent absence of any permanent growth structures. It was thought that when lobsters and other crustaceans molt, they shed all calcified body parts that might record annual growth bands.

[Researchers] took a closer look at lobsters, snow crabs, northern shrimp and sculptured shrimp. They found that growth rings, in fact, could be found in the eyestalk - a stalk connected to the body with an eyeball on the end - of lobsters, crabs and shrimp. In lobsters and crabs, the rings were also found in the so-called "gastric mills," parts of the stomach with three teeth-like structures used to grind up food.

http://www.huffingtonpost.com/huff-wires/20121130/us-lobster-aging/

Source:
http://www.fightaging.org/archives/2012/11/a-method-of-determining-lobster-age.php

The thyroid gland carries out a number of important functions, responding to changing conditions by varying its production of thyroid hormones that alter the behavior of metabolism elsewhere in the body. The behavior of the thyroid changes with age, but in a sufficiently subtle and varying manner to make its role in aging a challenging thing to study. Nonetheless, there is at this point enough data to conclude that some forms of reduced thyroid function tend to associate with increased longevity in a number of species.

This also ties in with other lines of research. Calorie restriction, for example, reduces thyroid hormone levels in the course of extending life and improving health. A predisposition to low thyroid hormone levels appear to be inherited in long-lived families. And so forth.

Here is a short and very readable open access review paper that looks at thyroid function in the context of aging and longevity:

The thyroid gland and the process of aging; what is new?

The endocrine system and particular endocrine organs, including the thyroid, undergo important functional changes during aging. The prevalence of thyroid disorders increases with age and numerous morphological and physiological changes of the thyroid gland during the process of aging are well-known.

Intriguingly, decreased thyroid function, as well as thyrotropin (TSH) levels - progressively shifting to higher values with age - may contribute to the increased lifespan. [The] most striking findings concerning potential contribution of TSH and thyroid hormones to lifespan regulation, were obtained in the studies performed on centenarians (and almost centenarians). In 2009, Atzmon et al. published the results of studies on thyroid disease-free population of Ashkenazi Jews, characterized by exceptional longevity (centenarians). They have observed higher serum TSH level in these subjects as compared to the control group. [Moreover], the authors have observed an inverse correlation between FT4 and TSH levels in centenarians and [controls], and finally, they have distinctly concluded that increased serum TSH is associated with extreme longevity

The above-mentioned inverse correlation between FT4 and TSH in centenarians may suggest a potential role of decreased thyroid function in lifespan regulation, leading to remarkable longevity. Such a hypothesis seems to have been confirmed by the findings obtained in the Leiden Longevity Study, demonstrating the associations between low thyroid activity and exceptional familial longevity.

It should be stressed that reduced thyroid function with low levels of T4 is associated with extended longevity also in animals. For example, a very severe thyroid hypofunction with reduced core body temperature, as observed in Ames dwarf (df/df) and Snell mice [is] considered to substantially contribute to remarkable longevity in these rodents. [The] findings in animals are consistent with the results obtained in humans and may confirm a relevant role of thyroid hypofunction in lifespan extension.

Source:
http://www.fightaging.org/archives/2012/11/the-association-of-reduced-thyroid-function-with-longevity.php

Metabolism is a very complex set of overlapping mechanisms, feedback loops, and networks of protein interactions. So even if there are only a few core methods of extending life by altering metabolism in a species, we should expect to see scores of different ways to trigger some or all of that alteration - and with widely varying side-effects. This is one of the present challenges facing those researchers who focus on how metabolism and genes determine natural variations in longevity: mapping it all for any one species is a vast task.

Here is one example of ongoing research drawn from among the many ways to make flies live longer:

Up-regulation of kynurenine (KYN) pathway of tryptophan (TRP) was suggested as one of the mechanisms of aging and aging-associated disorders. Genetic and pharmacological impairment of TRP - KYN metabolism resulted in prolongation of life span in Drosophila models.

Minocycline, an antibiotic with anti-inflammatory, antioxidant and neuroprotective properties independent of its antibacterial activity, inhibited KYN formation from TRP. Since minocycline is the only FDA approved for human use medication with inhibitory effect on TRP - KYN metabolism, we were interested to study minocycline effect on life- and health-spans in Drosophila model.

Minocycline prolonged mean, median and maximum life span of wild-type Oregon Drosophila melanogaster of both genders [and] might be a promising candidate drug for anti-aging intervention. [The] role of TRP - KYN metabolism in the mechanisms of minocycline-effect on life- and health-span might be elucidated by the future assessment of minocycline effects in Drosophila mutants naturally or artificially knockout for genes impacting the key enzymes of KYN pathway of TRP metabolism.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23185716

Source:
http://www.fightaging.org/archives/2012/11/kynurenine-tryptophan-metabolism-and-fly-longevity.php