楊乃成Nae-Cherng Yang鄭雅心Ya-Xin Zheng營養學系2026-03-249999-12-3120202020-07-21https://handle.ncl.edu.tw/11296/xp889mhttps://scholars.csmu.edu.tw/handle/123456789/7113肌醇 (inositol)一度被認為是維生素B8，但因人體可由葡萄糖自行合成，因此，目前已不再歸類為B群維生素之一，但事實上，缺乏肌醇會導致哺乳動物肝臟中三酸甘油酯及膽固醇大量累積，顯示它仍是重要的營養素。肌醇具有9種異構體，其中myo-Inositol (MI)是自然界及人體中主要的肌醇形式，研究發現MI具有許多的生理功效，包括：抗氧化、抗神經退化、抗憂鬱、抗糖尿病及治療多囊性卵巢症候群等，然而MI是否具有抗衰老的作用目前並不清楚？而且已知線蟲調控壽命主要有五條傳訊的路徑(1) insulin/insulin-like growth factor-1 signaling (IIS pathway)、(2) Sirtuin pathway、(3) TOR pathway、(4) AMPK pathway、(5) JNK pathway等，然而，MI可以藉由上述何種路徑延長線蟲壽命，目前亦不清楚？因此，本研究目的在於以探討MI延長線蟲壽命的能力與機制，我們以N2線蟲的生命期試驗探討MI對壽命影響，以body bends、pharyngeal pumping及線蟲 red autofluorescence 作為衰老的輔助指標，結果顯示MI具有延長線蟲壽命的作用，並且可以改善老化的輔助指標。進一步的研究結果發現MI可延長sir-2.1突變株壽命，但不能延長akt-1、jnk-1、daf-15、aak-2及daf-16 突變株壽命，並且MI可降低PI3K、TOR和Raptor蛋白表現，以及增加JNK和AMPK的磷酸化及降低Akt磷酸化。綜合以上顯示MI經由IIS、TOR、AMPK、JNK等路徑傳訊至DAF-16轉錄因子以延長壽命。Inositol was previously considered to be vitamin B8. However, because our body can synthesize it, so it is no longer classified as B vitamins. In fact, inositol deficiency causes large accumulation of triacylglycerol and cholesterol, showing that myo-inositol (MI) is an important nutrient. Inositol has 9 isomers, of which MI is the main form of inositol in nature and the human body. Studies have shown that MI has many physiological effects, including anti-oxidation, anti-neurodegeneration, anti-depression, anti-diabetic, and treatment of polycystic ovary syndrome. However, whether MI has anti-aging effects is still unclear to date. Moreover, there are five main pathways to regulate the lifespan of C. elegans, (1) insulin/insulin-like growth factor-1 signaling (IIS pathway), (2) Sirtuin pathway (3) TOR pathway (4) AMPK pathway (5 ) JNK pathway. It is also not clear that MI can extend the lifespan of C. elegans through which pathway. Therefore, the purpose of this study is to explore the ability and mechanisms of inositol to extend the lifespan of C. elegans. We used C. elegans strain N2 to explore the lifespan-extension ability of MI, and used body bends, pharyngeal pumping, and red autofluorescence as accessory indicators of aging. The results showed that MI could extend the lifespan of C. elegans and improve the indicators of aging. Furthermore, MI could extend the lifespan of sir-2.1 mutants, but could not extend the lifespan of akt-1, jnk-1, daf-15, aak-2, and daf-16 mutants. MI could reduce the expressions of PI3K, TOR and Raptor proteins and increase the phosphorylation of JNK and AMPK, and decrease the phosphorylation of Akt. These results demonstrate that MI can extend the lifespan of C. elegans through IIS, TOR, AMPK, and JNK pathways to promote DAF-16.myo-Inositol抗衰老IISTORAMPKJNK氧化壓力anti-agingoxidative stressthesis