加州大学旧金山分校Cynthia Kenyon等人发现，增加线虫(C.elegans)饮食中的葡萄糖含量，线虫的平均寿命减少20%。通过跟踪线虫的胰岛素信号作用，研究人员发现胰岛素信号能够阻断延长生命其他分子通路。由于人类和线虫在胰岛素信号通路方面有许多相似之处，所以该研究或许能够解释换肥胖症和2型糖尿病的分子机制。这篇研究报告发表于11月版Cell Metabolism杂志上。
自上世纪90年代初，研究人员就发现线虫基因(如daf-2基因)发生某些突变能够使其寿命延长一倍，而这些突变都影响胰岛素信号。寿命的延长还取决于“FOXO转录因子”家族其中的一个DAF-16蛋白和热休克因子HSF-1。
通过给线虫长期提供稳定的含葡萄糖的饮食的实验，研究人员发现，线虫负责转运甘油的水通道蛋白(aquaporin channel)明显减少，而甘油是线虫自身产生葡萄糖过程中所必须的分子。
针对上述实验现象，研究人员虽然到目前为止，还不完全清楚葡萄糖缩短线虫寿命的分子机制，但是他们认为，由于老鼠和人类的水通道蛋白转运甘油的能力可通过胰岛素下调，这增加了高葡萄糖饮食缩短寿命的可能性。反之，低血糖指数的饮食或许能够延长人类的寿命。（生物谷Bioon.com）
长寿相关研究：
Nature：反复禁食可延长线虫寿命
Science：蠕虫燃烧油脂以增长寿命
Molecular Cell：能延长寿命和降低胆固醇的基因
Nature：Sirtuins与寿命调控之间的关系
Nature：抗抑郁药能延长线虫寿命 有助推动人类抗老化研究
生物谷推荐原始出处：
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.
