New study reveals why restricting calories may lead to longevity
Finding a way to increase the lifespan of humans has been a subject of interest for a very long time. Since seventy years ago, scientists have known that to increase the life of animals they could cut the caloric intake by 30-40%, but they didn't know why this was effective. Recently though they have found that two enzymes, SIRT3 and SIRT4, may be the causes for the longevity. These enzymes are located in the mitochondria and when calories are cut, the levels of these enzymes increase, which strengthens the mitochondria. The enzymes prevent flagging mitochodria from developing pores that allow proteins that trigger apoptosis to seep into the rest of the cell.
If a diet with lowered levels of calories will activate a gene inside cells that codes for an enzyme, NAMPT(nicotinamide phosphoribosyltransferase). An increase in NAMPT will in turn cause NAD to be produced. The NAD plays a key role in cellular metabolism and signaling. With more NAD, the SIRT3 and SIRT4 genes are activated. While it is not known how these enzymes help with mitochondria energy output, scientists do know that events leading up to cell death are delayed with the prescence of the enzymes.
The next step for scientists is to create a "supermouse" that will overexpress NAMPT to see if the animal lives longer and is more resistant to disease than other unaltered mice.
Remembering the SNBAL that we did a few weeks ago, this article really interested me. It provides some effective evidence for mitochondria being a source for aging. With this new information, more experiments with aging can be done and the mitochondria can be specifically targeted to stop cell death. The question that remains though, are humans willing enough to make extreme changes to their diet in order to live longer?
http://www.sciam.com/article.cfm?articleID=242CBE56-E7F2-99DF-37DEAE209E877BFB&chanID=sa011
If a diet with lowered levels of calories will activate a gene inside cells that codes for an enzyme, NAMPT(nicotinamide phosphoribosyltransferase). An increase in NAMPT will in turn cause NAD to be produced. The NAD plays a key role in cellular metabolism and signaling. With more NAD, the SIRT3 and SIRT4 genes are activated. While it is not known how these enzymes help with mitochondria energy output, scientists do know that events leading up to cell death are delayed with the prescence of the enzymes.
The next step for scientists is to create a "supermouse" that will overexpress NAMPT to see if the animal lives longer and is more resistant to disease than other unaltered mice.
Remembering the SNBAL that we did a few weeks ago, this article really interested me. It provides some effective evidence for mitochondria being a source for aging. With this new information, more experiments with aging can be done and the mitochondria can be specifically targeted to stop cell death. The question that remains though, are humans willing enough to make extreme changes to their diet in order to live longer?
http://www.sciam.com/article.cfm?articleID=242CBE56-E7F2-99DF-37DEAE209E877BFB&chanID=sa011
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