国内团队:肠道菌群介导高盐饮食诱导的高血压
创作:szx 审核:szx 03月01日
  • 移植健康大鼠的粪便菌群可显著降低高盐饮食诱导的高血压(hSIH)大鼠的血压,而移植hSIH大鼠的粪便菌群可显著升高健康大鼠的血压;
  • 高盐饮食显著改变了大鼠的肠道菌群组成,降低了脆弱拟杆菌及肠道中的花生四烯酸水平,从而增加血清及肠道中的皮质酮水平以促进血压的提升;
  • 在高血压患者中也可发现,粪便中的脆弱拟杆菌YCH46显著减少,血清及肠道中的皮质酮水平显著升高。
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szx
肠道菌群与高盐饮食诱导的高血压相关,但背后的机制尚不清晰。来自山东大学齐鲁医院的张群业团队及山东省立医院的王哲团队在Circulation Research上发表的一项最新研究,报道了肠道菌群介导高盐饮食诱导高血压产生的机制:高盐饮食通过改变肠道菌群的组成及代谢,减少脆弱拟杆菌,从而提升皮质酮水平以促进高血压,而脆弱拟杆菌可通过其代谢产物花生四烯酸抑制皮质酮的产生。
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Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension

在高盐诱导的高血压中,肠道菌群通过调节皮质酮的合成调控血压

10.1161/CIRCRESAHA.119.316394

02-13, Article

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Rationale: High-salt diet (HSD) is one of the most important risk factors for hypertension. Intestinal flora has been reported to be associated with high salt-induced hypertension (hSIH). However, the detailed roles of intestinal flora in hSIH pathogenesis have not yet been fully elucidated.
Objective: To reveal the roles and mechanisms of intestinal flora in hSIH development.
Methods and Results: The above-mentioned issues were investigated using various techniques including 16S rRNA gene sequencing, untargeted metabolomics, selective bacterial culture and fecal microbiota transplantation (FMT). We found that HSD induced hypertension in Wistar rats. The fecal microbiota of healthy rats could dramatically lower blood pressure (BP) of hypertensive rats, while the fecal microbiota of hSIH rats had opposite effects. The composition, metabolism and interrelationship of intestinal flora in hSIH rats were considerably reshaped, including the increased corticosterone level and reduced Bacteroides and arachidonic acid (AA) levels, which tightly correlated with BP. The serum corticosterone level was also significantly increased in rats with hSIH. Furthermore, the above abnormalities were confirmed in patients with hypertension. The intestinal Bacteroides fragilis (B. fragilis) could inhibit the production of intestinal-derived corticosterone induced by HSD through its metabolite AA.
Conclusions: hSIH could be transferred by FMT, indicating the pivotal roles of intestinal flora in hSIH development. HSD reduced the levels of B. fragilis and AA in the intestine, which increased intestinal-derived corticosterone production and corticosterone levels in serum and intestine, thereby promoting BP elevation. This study revealed a novel mechanism different from inflammation/immunity by which intestinal flora regulated BP, namely intestinal flora could modulate BP by affecting steroid hormone levels. These findings enriched the understanding of the function of intestinal flora and its effects on hypertension.

First Authors:
Xuefang Yan

Correspondence Authors:
Zhe Wang,Qunye Zhang

All Authors:
Xuefang Yan,Jiajia Jin,Xinhuan Su,Xianlun Yin,Jing Gao,Xiaowei Wang,Shucui Zhang,Peili Bu,Mansen Wang,Yun Zhang,Zhe Wang,Qunye Zhang

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