Kazak faecal microbiota transplantation induces short-chain fatty acids that promote glucagon-like peptide-1 secretion by regulating gut microbiota in db/db mice,Pharmaceutical Biology

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Kazak faecal microbiota transplantation induces short-chain fatty acids that promote glucagon-like peptide-1 secretion by regulating gut microbiota in db/db mice
Pharmaceutical Biology ( IF 3.8 ) Pub Date : 2021-08-15 , DOI: 10.1080/13880209.2021.1954667
Xue Han ₁ , Ye Wang ₁ , Peipei Zhang ₂ , Manli Zhu ₃ , Ling Li ₄ , Xinmin Mao _{5,

6} , Xiaoting Sha ₁ , Linlin Li _{1,

5,

7}

Affiliation

Abstract

Context

Faecal microbiota transplantation (FMT) from Kazak individuals with normal glucose tolerance (KNGT) significantly reduces plasma glycolipid levels in type 2 diabetes mellitus db/db mice. However, the mechanism behind this effect has not been reported.

Objective

To study the mechanism of improved glycolipid disorders in db/db mice by FMT from a KNGT donor.

Materials and methods

The normal diet group consisted of db/m mice orally administered 0.2 mL phosphate buffer saline (PBS) (db/m + PBS). For the db/db + PBS (Vehicle) and db/db + KNGT (FMT intervention group) groups, db/db mice received oral 0.2 mL PBS or faecal microorganisms from a KNGT donor, respectively. All mice were treated daily for 0, 6 or 10 weeks. Faecal DNA samples were sequenced and quantified using 16S rRNA gene sequencing and RT-qPCR, respectively. Short-chain fatty acid (SCFA) levels in the mouse faeces were determined by gas chromatography. G protein-coupled receptor 43 (GPR43) and glucagon-like peptide-1 (GLP-1) expression levels were determined.

Results

FMT intervention significantly increased the relative abundance of Bacteroides uniformis (0.038%, p < 0.05). Clostridium levels (LogSQ) were increased (p < 0.01), while Mucispirillum schaedleri levels (LogSQ) were decreased (p < 0.01). Acetate and butyrate levels in the faeces were significantly increased (acetate; butyrate: 22.68 ± 1.82 mmol/L; 4.13 ± 1.09 mmol/L, p < 0.05). GPR43 mRNA expression and GLP-1 protein expression increased in colon tissue (p < 0.05).

Discussion and conclusions

Mechanistically, FMT-KNGT could improve glycolipid disorders by changing the bacterial composition responsible for producing SCFAs and activating the GPR43/GLP-1 pathway.

中文翻译：

哈萨克粪便微生物群移植诱导短链脂肪酸通过调节 db/db 小鼠肠道微生物群促进胰高血糖素样肽-1 的分泌

摘要

语境

来自葡萄糖耐量正常 (KNGT) 的哈萨克斯坦人的粪便微生物群移植 (FMT) 显着降低了 2 型糖尿病db/db小鼠的血浆糖脂水平。然而，这种效应背后的机制尚未见报道。

客观的

研究通过来自 KNGT 供体的 FMT改善db/db小鼠糖脂紊乱的机制。

材料和方法

正常饮食组由db/m小鼠口服 0.2 mL 磷酸盐缓冲液 (PBS) ( db/m + PBS ) 组成。对于db/db + PBS（车辆）和db/db + KNGT（FMT 干预组）组，db/db小鼠分别接受来自 KNGT 供体的口服 0.2 mL PBS 或粪便微生物。所有小鼠每天治疗 0、6 或 10 周。粪便 DNA 样本分别使用 16S rRNA 基因测序和 RT-qPCR 进行测序和定量。通过气相色谱法测定小鼠粪便中的短链脂肪酸 (SCFA) 水平。测定了 G 蛋白偶联受体 43 (GPR43) 和胰高血糖素样肽 1 (GLP-1) 的表达水平。

结果

FMT 干预显着增加了均匀拟杆菌的相对丰度(0.038%, p < 0.05)。梭状芽胞杆菌水平（LogSQ）增加（p < 0.01），而Mucispirillum schaedleri水平（LogSQ）降低（p < 0.01）。粪便中的乙酸盐和丁酸盐水平显着增加（乙酸盐；丁酸盐：22.68 ± 1.82 mmol/L；4.13 ± 1.09 mmol/L，p < 0.05）。结肠组织中GPR43 mRNA表达和GLP-1蛋白表达增加（p < 0.05）。