Characterisation of gut microbiota of obesity and type 2 diabetes in a rodent model

被引:13
|
作者
Ibrahim, Khalid S. [1 ,2 ]
Bourwis, Nowara [1 ]
Dolan, Sharron [1 ]
Lang, Sue [1 ,3 ]
Spencer, Janice [1 ]
Craft, John A. [1 ]
机构
[1] Glasgow Caledonian Univ, Dept Biol & Biomed Sci, Glasgow G4 0BA, Lanark, Scotland
[2] Univ Zakho, Fac Sci, Dept Biol, Zakho Int Rd, Duhok, Kurdistan Regio, Iraq
[3] Leeds Beckett Univ, Sch Clin & Appl Sci, Portland Bldg,City Campus, Leeds LS1 3HE, W Yorkshire, England
基金
英国工程与自然科学研究理事会;
关键词
butyrate; inflammatory molecules; microbiome; obesity; Type; 2; diabetes; HIGH-FAT DIET; INTESTINAL MICROBIOTA; MOLECULAR ANALYSIS; RATS; MODULATION; BUTYRATE; ONSET;
D O I
10.12938/bmfh.2019-031
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Various studies have suggested that the gut microbiome interacts with the host and may have a significant role in the aetiology of obesity and Type 2 Diabetes (T2D). It was hypothesised that bacterial communities in obesity and T2 D differ from control and compromise normal interactions between host and microbiota. Obesity and T2D were developed in rats by feeding a high-fat diet or a high-fat diet plus a single low-dose streptozotocin administration, respectively. The microbiome profiles and their metabolic potentials were established by metagenomic 16S rRNA sequencing and bioinformatics. Taxonomy and predicted metabolism-related genes in obesity and T2D were markedly different from controls and indeed from each other. Diversity was reduced in T2D but not in Obese rats. Factors likely to compromise host intestinal, harrier integrity were found in Obese and T2D rats including predicted, decreased bacterial butyrate production. Capacity to increase energy extraction via ABC-transporters and carbohydrate metabolism were enhanced in Obese and T2D rats. T2D was characterized by increased p ruin flammatory molecules. While obesity and T213 show distinct differences, results suggest that in both conditions Bacteroides and Blautia species were increased indicating a possible mechanistic link.
引用
收藏
页码:65 / 74
页数:10
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