加州大學(xué)舊金山分校Cynthia Kenyon等人發(fā)現(xiàn)，增加線蟲(C.elegans)飲食中的葡萄糖含量,，線蟲的平均壽命減少20%,。通過(guò)跟蹤線蟲的胰島素信號(hào)作用，研究人員發(fā)現(xiàn)胰島素信號(hào)能夠阻斷延長(zhǎng)生命其他分子通路,。由于人類和線蟲在胰島素信號(hào)通路方面有許多相似之處,，所以該研究或許能夠解釋換肥胖癥和2型糖尿病的分子機(jī)制。這篇研究報(bào)告發(fā)表于11月版Cell Metabolism雜志上,。
自上世紀(jì)90年代初,，研究人員就發(fā)現(xiàn)線蟲基因(如daf-2基因)發(fā)生某些突變能夠使其壽命延長(zhǎng)一倍，而這些突變都影響胰島素信號(hào),。壽命的延長(zhǎng)還取決于“FOXO轉(zhuǎn)錄因子”家族其中的一個(gè)DAF-16蛋白和熱休克因子HSF-1,。
通過(guò)給線蟲長(zhǎng)期提供穩(wěn)定的含葡萄糖的飲食的實(shí)驗(yàn)，研究人員發(fā)現(xiàn),，線蟲負(fù)責(zé)轉(zhuǎn)運(yùn)甘油的水通道蛋白(aquaporin channel)明顯減少,，而甘油是線蟲自身產(chǎn)生葡萄糖過(guò)程中所必須的分子。
針對(duì)上述實(shí)驗(yàn)現(xiàn)象,，研究人員雖然到目前為止，還不完全清楚葡萄糖縮短線蟲壽命的分子機(jī)制,，但是他們認(rèn)為,，由于老鼠和人類的水通道蛋白轉(zhuǎn)運(yùn)甘油的能力可通過(guò)胰島素下調(diào)，這增加了高葡萄糖飲食縮短壽命的可能性,。反之,，低血糖指數(shù)的飲食或許能夠延長(zhǎng)人類的壽命。（生物谷Bioon.com）
長(zhǎng)壽相關(guān)研究：
Nature：反復(fù)禁食可延長(zhǎng)線蟲壽命
Science：蠕蟲燃燒油脂以增長(zhǎng)壽命
Molecular Cell：能延長(zhǎng)壽命和降低膽固醇的基因
Nature：Sirtuins與壽命調(diào)控之間的關(guān)系
Nature：抗抑郁藥能延長(zhǎng)線蟲壽命 有助推動(dòng)人類抗老化研究
生物谷推薦原始出處：
Cell Metabolism,4 November 2009 doi:10.1016/j.cmet.2009.10.003
Glucose Shortens the Life Span of C. elegans by Downregulating DAF-16/FOXO Activity and Aquaporin Gene Expression
Seung-Jae Lee1, 2, 3, 4, Coleen T. Murphy1, 5 and Cynthia Kenyon1, ,
1 Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA
2 Division of Molecular and Life Science, Pohang University of Science and Technology, Pohang, Kyungbuk, 790-784, South Korea
3 School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Kyungbuk, 790-784, South Korea
4 World Class University Information Technology Convergence Engineering, Pohang University of Science and Technology, Pohang, Kyungbuk, 790-784, South Korea
Many studies have addressed the effect of dietary glycemic index on obesity and diabetes, but little is known about its effect on life span itself. We found that adding a small amount of glucose to the medium (2%) shortened the life span of C. elegans by inhibiting the activities of life span-extending transcription factors that are also inhibited by insulin signaling: the FOXO family member DAF-16 and the heat shock factor HSF-1. This effect involved the downregulation of an aquaporin glycerol channel, aqp-1. We show that changes in glycerol metabolism are likely to underlie the life span-shortening effect of glucose and that aqp-1 may act cell nonautonomously as a feedback regulator in the insulin/IGF-1-signaling pathway. Insulin downregulates similar glycerol channels in mammals, suggesting that this glucose-responsive pathway might be conserved evolutionarily. Together, these findings raise the possibility that a low-sugar diet might have beneficial effects on life span in higher organisms.
