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Caloric Restriction: Difference between revisions
→Activation of Sirtuin-1 and Reduced Expression of the mTOR Receptor
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In contrast to the free radical theory, it is assumed that an increased formation of reactive oxygen species in the mitochondria, associated with caloric restriction, causes an adaptive response that enhances stress resistance.<ref name="PMID20350594">PMID 20350594</ref> | In contrast to the free radical theory, it is assumed that an increased formation of reactive oxygen species in the mitochondria, associated with caloric restriction, causes an adaptive response that enhances stress resistance.<ref name="PMID20350594">PMID 20350594</ref> | ||
===Activation of Sirtuin-1 and Reduced Expression of the mTOR Receptor === | ===Activation of Sirtuin-1 and Reduced Expression of the mTOR Receptor === | ||
Signal-regulating enzymes such as [[SIRT1|Sirtuin-1 (Sirt1)]] in mammals, or [[SIRT2|Sirtuin ''Sir2'']] in yeasts, may play a role. | Signal-regulating enzymes such as [[SIRT1|Sirtuin-1 (Sirt1)]] in mammals, or [[SIRT2|Sirtuin ''Sir2'']] in yeasts, may play a role.{{pmid|25349818}} The cells of calorically restricted test animals produce Sirt1 in larger quantities.{{pmid|19713122}} An increased production of Sirt1, in turn, reduces the expression of the mTOR receptor (''mammalian Target of Rapamycin''),{{pmid|20169165}} which is also associated with the aging process. The lifespan of mice can be significantly extended by administering [[Rapamycin]], which docks to the mTOR receptor.{{pmid|20331443}}{{pmid|19587680}} [[Melatonin]] is also being studied due to its activation of Sirtuin.{{pmid|25824609}} | ||
==Benefits of Caloric Restriction== | ==Benefits of Caloric Restriction== | ||