Studies Of Caloric Restriction, Resveratrol And Sirt1 Demonstrate A ?Metabotype’ Continuum From Cellular Rejuvenation To Aging To Cancer
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way to have the appearance of a Lamarckian outcome, is for pre-adaptation to have arisen from numerous, widely spaced, earlier or many, highly selective, recent exposures to a phenomenon. The more gene systems affected in a more orchestrated fashion, the more ancient and more protracted the system must be. Open ended circular arguments apply to life, because life has ‘been there’ before, especially in the case of famine, and because, successful gene systems replicate and fan out over time. In regards to the subject focus of this document, there appears to be a much more ancient and a much larger and much more controlled famine gene manipulation system than epigenetics at work. I broached these topics to put forth the notion that ancient systems, such as intermediary metabolism, mitochondrial function and anciently occurring phenomena, such as feast and famine, grew along with the growth of the metabolic pathways themselves. Whole suites of genes are involved with their control, but over time the system evolves to arrive at a relatively few fixed sets of ‘tried and true’ tactics that have become, more or less, successful fixed response systems. Other, more flexible life components, such as length of time as a juvenile, or length of life as an adult, may be operating in an intermediate time spectrum, as they are responding to phenomena much longer than epigenetics, but much shorter than raw metabotype, although all three systems outlined, here, from a feast and famine standpoint, can leave their mark upon metabotype expression. My point is this: even though there are hundreds of cell growth factors, the unique mixes, of which, tell each cell type when and how fast to grow and divide, there seems to be a veritable paucity of system(s) setting mitochondrial biogenesis in motion, with its apparent requisite reestablishment of the 5/95 glycolytic/Krebs ATP production ratios, and the resultant catabolic/anabolic rate shift. This rejuvenating biogenic system appears to paint with a broad brush, saying essentially ‘on’ in juvenile cells, ‘off’ in adult cells, and when in the ‘off’ position, mitochondria slowly age (as in humans), or rapidly age (as in mice), toward the inefficient cancer-like metabotype. This becomes a precancerous, or hyperplasic condition awaiting growth signal and signal related mutations, to transform it into the cancerous state. Amazingly, the juvenile system can be turned back on in adult cells, but only when the organism is in dire straights of a type recurrent from the dawn of metabolic evolution. Interestingly, most mammals fail to ovulate if they are not carrying enough fat supply, so caloric restriction carries extended life in exchange for the loss procreative capacity, thus allowing species replacement numbers to be deferred to a more nutrient plush future. Conversely, when feast times return, fat storage ensues, high ATP production efficiency is no longer a life sustaining requirement, and after a few procreative cycles, the now shorter lived adults, are disposed of. It is rather interesting that nature has also found a mechanism for failing mitochondria to act in a metabolic default toward cell growth, the caveat of it, being linked to life saving energy supply availability, on the one hand, and the potential to assist in the death dealing carcinogenic process, on the other. There does not seem to be any real overt need to modify this ancient system, save to change the length of the juvenile and adult stages to suit the environmental conditions demanding such. These life stage length differences between mice, dogs, horses, humans etc. are independent of metabolic rate, body size, the brain to body
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