Whon Tae Woong, Shin Na-Ri, Jung Mi-Ja, Hyun Dong-Wook, Kim Hyun Sik, Kim Pil Soo, Bae Jin-Woo
Department of Life and Nanopharmaceutical Sciences and Department of Biology, Kyung Hee University , Seoul, Republic of Korea.
Antioxid Redox Signal. 2017 Dec 1;27(16):1361-1380. doi: 10.1089/ars.2016.6790. Epub 2017 May 24.
Changes in the composition of the gut microbiota contribute to the development of obesity and subsequent complications that are associated with metabolic syndrome. However, the role of increased numbers of certain bacterial species during the progress of obesity and factor(s) controlling the community structure of gut microbiota remain unclear. Here, we demonstrate the inter-relationship between Drosophila melanogaster and their resident gut microbiota under chronic high-sugar diet (HSD) conditions.
Chronic feeding of an HSD to Drosophila resulted in a predominance of resident uracil-secreting bacteria in the gut. Axenic insects mono-associated with uracil-secreting bacteria or supplemented with uracil under HSD conditions promoted larval development. Redox signaling induced by bacterial uracil promoted larval growth by regulating sugar and lipid metabolism via activation of p38a mitogen-activated protein kinase.
The present study identified a new redox-dependent mechanism by which uracil-secreting bacteria (previously regarded as opportunistic pathobionts) protect the host from metabolic perturbation under chronic HSD conditions.
These results illustrate how Drosophila and gut microbes form a symbiotic relationship under stress conditions, and changes in the gut microbiota play an important role in alleviating deleterious diet-derived effects such as hyperglycemia. Antioxid. Redox Signal. 27, 1361-1380.
肠道微生物群组成的变化有助于肥胖的发展以及与代谢综合征相关的后续并发症。然而，在肥胖进展过程中某些细菌种类数量增加的作用以及控制肠道微生物群群落结构的因素仍不清楚。在此，我们展示了在慢性高糖饮食（HSD）条件下黑腹果蝇与其肠道内常驻微生物群之间的相互关系。
给果蝇长期喂食HSD导致肠道内主要是分泌尿嘧啶的常驻细菌。在HSD条件下，与分泌尿嘧啶的细菌单联或补充尿嘧啶的无菌昆虫促进了幼虫发育。细菌尿嘧啶诱导的氧化还原信号通过激活p38a丝裂原活化蛋白激酶调节糖和脂质代谢，从而促进幼虫生长。
本研究确定了一种新的氧化还原依赖性机制，通过该机制，分泌尿嘧啶的细菌（以前被视为机会性致病共生菌）在慢性HSD条件下保护宿主免受代谢紊乱。
这些结果说明了果蝇和肠道微生物在应激条件下如何形成共生关系，并且肠道微生物群的变化在减轻诸如高血糖等有害饮食衍生效应方面发挥重要作用。《抗氧化与氧化还原信号》27, 1361 - 1380。
