寿命とニコチンアミド(高齢者とB群ビタミン)

抄録

The research on the relation between the reactions of acetylation and deacetylation of histone and suppression and activation of the transcription has been recently preceded. In 1999, it was reported that yeast which had one extra copy of Sir2 was found having 1.4 times longevity, while, the mutant to lack Sir2 being shortened to 1/2 compared with the wild types. In addition, in 2002, it was clarified that Sir2 (=NAD^+-dependent histone deacetylase) was inhibited by nicotinamide that was one of the products. In 2003, as for the extension of the longevity that induced by the energy restriction, it was reported that it happened through increasing the appearance of PNC1 (a gene that codes nicotinamidase), and however, the effect disappeared due to the lack of Sir2. Well, the mammal has the sirtuin (SIRT) family, and it is known that SIRT1 is homolog that is the nearest to the yeast Sir2. In 2004, it was reported that the appearance of SIRT1 had increased with the brain, fat tissues, the kidney, and the liver, when the rat was kept for 12 months under the energy restriction of 60%. From these reports, I have thought that it becomes a key that extends longevity that the relation between the Sir2 protein (NAD^+-dependence histone deacetylase) and nicotinamidase controls aging. The nicotinamide metabolism in the nuclei was presumed in relation to Sir2 and nicotinamidase. Moreover, it was reported that the activities of rat liver nicotinamidase, and nicotinamide methyltransferase which is another nicotinamide metabolizing enzyme were increased by the energy restriction. In mammals, the catabolism of nicotinamide being increased by the dietary restriction (limitation of amount of level that the weight of the maturity rat is maintained constantly) becomes clear.