Manipulating Fat in the Context of Slowing Aging

Researchers have established to a more than reasonable degree that fat is important in longevity and aging. A compelling experiment in mice, for example, demonstrates that less visceral fat means a longer life. Then we have the link between fat and chronic inflammation, and the strong correlations between excess fat tissue and all of the common age-related conditions.

Given all of this evidence, it shouldn't be surprising that at least some of those researchers interested in slowing down the aging process are thinking in terms of changing the fundamental processes of fat metabolism. One such paper caught my eye today, and I thought I'd share:

Protein kinase A signaling as an anti-aging target:

As one of its many functions, protein kinase A (PKA) plays a key role in the regulation of metabolism and triglyceride storage. The PKA pathway has become of great interest to the study of aging, since mutations that cause a reduction in PKA signaling have been shown to extend lifespan in yeast, and to both delay the incidence and severity of age-related disease, and to promote leanness and longevity, in mice.

There is increasing interest in the potential for the inhibition or redistribution of adiposity to attenuate aging, since obesity is associated with impaired function of most organ systems, and is a strong risk factor for shortened life span. Its association with coronary heart disease, hypertension, type 2 diabetes, cancer, sleep apnea and osteoarthritis is leading to its accession as a major cause of global ill health. Therefore, gene signaling pathways such as PKA that promote adiposity are potential inhibitory targets for aging intervention. Since numerous plant compounds have been found that both prevent [creation of fat tissue] and inhibit PKA signaling, a focused investigation into their effects on biological systems and the corresponding molecular mechanisms would be of high relevance to the discovery of novel and non toxic compounds that promote healthy aging.

You might recall that the stated context of the Longevity Dividend initiative is to add a handful of years to life, perhaps less than ten, over the next decade or two - a very modest goal that the founders felt was sufficiently close to the status quo to use in a push for large-scale public funding. There is evidence enough to suggest that the difference between more fat or less fat, or a more healthy or less healthy lifestyle can be as much a decade of life span. So within the Longevity Dividend paradigm, aiming to manipulate fat tissue makes sense.

By now it should go without saying that I think this is interesting, but the slow boat to China. The best way forward to extended healthy life is the Strategies for Engineered Negligible Senescence (SENS), or something very similar. This is a focus on repairing and reversing changes in our biochemistry rather than changing metabolism to slow the rate at which that damage occurs. You can look back in the archives for more on this topic:

It is likely to be easier and less costly to produce rejuvenation therapies than to produce a reliable and significant slowing of aging. A rejuvenation therapy doesn't require a whole new metabolism to be engineered, tested, and understood - it requires that we revert clearly identified changes to return to a metabolic model that we know works, as it's used by a few billion young people already. Those rejuvenation therapies will be far more effective than slowing aging in terms of additional years gained, since you can keep coming back to use them again and again. They will also help the aged, who are not helped at all by a therapy that merely slows aging.

ResearchBlogging.orgEnns LC, & Ladiges W (2010). Protein kinase A signaling as an anti-aging target. Ageing research reviews PMID: 20188216

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