DDS通过微生物组介导的饥饿信号促进长寿

Q2 Medicine
Haeri Choi , Sung Chun Cho , Young Wan Ha , Billie Ocampo , Shirley Park , Shiwen Chen , Christopher F. Bennett , Jeehae Han , Ryan Rossner , Jong-Sun Kang , Yun-ll Lee , Sang Chul Park , Matt Kaeberlein
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引用次数: 8

摘要

抗生素二氨基二苯砜(DDS)与其他抗生素联合使用,作为麻风病的一线治疗方法。此前有报道称DDS通过抑制丙酮酸激酶和降低线粒体功能延长秀丽隐杆线虫的寿命。在这里,我们报告了另一种作用机制,即DDS通过减少微生物组的叶酸产量来促进秀丽隐杆线虫的寿命。这导致蛋氨酸循环代谢物水平的改变,模拟二甲双胍的影响,并延长依赖于饥饿和缺氧诱导的含单加氧酶(FMO-2)的黄素的寿命。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

DDS promotes longevity through a microbiome-mediated starvation signal

DDS promotes longevity through a microbiome-mediated starvation signal

DDS promotes longevity through a microbiome-mediated starvation signal

DDS promotes longevity through a microbiome-mediated starvation signal

The antibiotic diaminodiphenyl sulfone (DDS) is used in combination with other antibiotics as a first line treatment for leprosy. DDS has been previously reported to extend lifespan in Caenorhabditis elegans through inhibition of pyruvate kinase and decreased mitochondrial function. Here we report an alternative mechanism of action by which DDS promotes longevity in C. elegans by reducing folate production by the microbiome. This results in altered methionine cycle metabolite levels mimicking the effects of metformin and lifespan extension that is dependent on the starvation- and hypoxia-induced flavin containing monoxygenase, FMO-2.

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来源期刊
Translational Medicine of Aging
Translational Medicine of Aging Medicine-Geriatrics and Gerontology
CiteScore
5.30
自引率
0.00%
发文量
2
审稿时长
103 days
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