粪菌移植通过调节 5-羟色胺合成缓解高脂饮食诱导肥胖大鼠的胃肠道转运。
Fecal Microbiota Transplantation Can Alleviate Gastrointestinal Transit in Rats with High-Fat Diet-Induced Obesity via Regulation of Serotonin Biosynthesis.
机构信息
Department of Gastroenterology, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China.
出版信息
Biomed Res Int. 2018 Oct 2;2018:8308671. doi: 10.1155/2018/8308671. eCollection 2018.
AIM
We tested the hypothesis that fecal microbiota transplantation (FMT) could regulate the biotransformation of bile acids, such as deoxycholic acid (DCA) and cholic acid (CA), which in turn regulate the biosynthesis of serotonin in the gut and relieve gastrointestinal dysmotility in high-fat diet- (HFD-) induced obesity in rats.
METHODS
Male Sprague-Dawley rats were randomly divided into the control diet group, HFD group, and HFD-fed with receiving FMT. HFD was fed for 12 weeks. At the end of two-week HFD, FMT was carried out for two weeks. The gastrointestinal transit, serotonin concentration, the expression of tryptophan hydroxylase 1 (TPH1) and serotonin reuptake transporter (SERT), and the levels of bile acids in intestinal contents were examined.
RESULTS
Compared with the control group, the gastrointestinal transit and small intestinal serotonin concentration of HFD-fed rats were increased. In HFD-fed rats, TPH1 protein expression was increased significantly, while SERT protein expression was decreased, but not significant. The levels of CA and DCA in intestinal contents were also significantly increased in HFD-fed rats compared with the control group. After HFD-fed rats receiving FMT treatment, the gastrointestinal transit, small intestinal serotonin concentration, and TPH1 expression were decreased, while SERT expression was not affected. Moreover, the levels of CA and DCA in intestinal contents were also decreased.
CONCLUSIONS
FMT could alleviate small intestinal transit in the HFD-fed rats by regulating the serotonin biosynthesis. In this process, CA and DCA may be related to the regulation of synthesis of serotonin.
目的
我们检验了这样一个假设，即粪便微生物群移植（FMT）可以调节胆汁酸的生物转化，如脱氧胆酸（DCA）和胆酸（CA），进而调节肠道中 5-羟色胺的生物合成，并缓解高脂肪饮食（HFD）诱导的肥胖大鼠的胃肠道动力障碍。
方法
雄性 Sprague-Dawley 大鼠被随机分为对照组、HFD 组和 HFD 喂养接受 FMT 组。HFD 喂养 12 周。在 HFD 喂养两周后，进行了两周的 FMT。检测了胃肠道转运、血清素浓度、色氨酸羟化酶 1（TPH1）和 5-羟色胺再摄取转运体（SERT）的表达以及肠内容物中胆汁酸的水平。
结果
与对照组相比，HFD 喂养大鼠的胃肠道转运和小肠血清素浓度增加。在 HFD 喂养大鼠中，TPH1 蛋白表达显著增加，而 SERT 蛋白表达减少，但不显著。与对照组相比，HFD 喂养大鼠的肠内容物中 CA 和 DCA 水平也显著增加。在接受 FMT 治疗的 HFD 喂养大鼠中，胃肠道转运、小肠血清素浓度和 TPH1 表达降低，而 SERT 表达不受影响。此外，肠内容物中 CA 和 DCA 的水平也降低了。
结论
FMT 可以通过调节 5-羟色胺的生物合成来缓解 HFD 喂养大鼠的小肠转运。在这个过程中，CA 和 DCA 可能与 5-羟色胺合成的调节有关。
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