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用阿月浑子(L.)进行饮食干预后糖尿病大鼠肠道微生物群的功能调节

Functional modulation of gut microbiota in diabetic rats following dietary intervention with pistachio nuts ( L.).

作者信息

Yanni Amalia E, Mitropoulou Gregoria, Prapa Ioanna, Agrogiannis Georgios, Kostomitsopoulos Nikolaos, Bezirtzoglou Eugenia, Kourkoutas Yiannis, Karathanos Vaios T

机构信息

Laboratory of Chemistry, Biochemistry, Physical Chemistry of Foods, Department of Nutrition and Dietetics, Harokopio University of Athens, Athens, Greece.

Laboratory of Applied Microbiology and Biotechnology, Department of Molecular Biology and Genetics, Democritus University of Thrace, Alexandroupolis, GR, 68100, Greece.

出版信息

Metabol Open. 2020 Jun 21;7:100040. doi: 10.1016/j.metop.2020.100040. eCollection 2020 Sep.

DOI:10.1016/j.metop.2020.100040
PMID:32812934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7424811/
Abstract

BACKGROUND

Gut microbiota holds a key-role in numerous biological functions and has emerged as a driving force for the development of diabetes. Diet contributes to gut microbiota diversity and functionality providing a tool for the prevention and management of the disease. The study aimed to investigate the effect of a dietary intervention with pistachio nuts, a rich source of monounsaturated fatty acids, dietary fibers and phytochemicals on gut microbiota composition in the rat model of Type 1 Diabetes.

METHODS

Male Wistar rats were randomly assigned into four groups: healthy animals which received control diet (CD) or pistachio diet (PD), and diabetic animals which received control diet (DCD) or pistachio diet (DPD) for 4 weeks. Plasma biochemical parameters were determined and histological examination of liver and pancreas was performed at the end of the dietary intervention. Adherent intestinal microbiota populations in jejunum, ileum, caecum and colon were analyzed. Fecal microbiota populations at the beginning and the end of the study were determined by microbiological analysis and 16S rRNA sequencing.

RESULTS

Diabetic animals of both groups exhibited high plasma glucose and low insulin concentrations, as well as characteristic pancreatic lesions. Pistachio supplementation significantly increased lactobacilli and bifidobacteria populations in jejunum, ileum and caecum ( < 0.05) and normalized microbial flora in all examined intestinal regions of diabetic animals. After 4 weeks of supplementation, populations of bifidobacteria and lactobacilli were increased in feces of both healthy and diabetic animals, while enterococci levels were decreased ( < 0.05). Next Generation Sequencing of fecal samples revealed increased and decreased counts of and , respectively, in healthy animals that received the pistachio diet. OTUs were higher in diabetic animals and increased over time in the pistachio treated groups, along with increased abundance of , and populations were elevated in healthy animals administered the pistachio nuts. Of note, relative abundance of was higher in healthy than in diabetic rats ( < 0.05).

CONCLUSION

Dietary pistachio restored normal flora and enhanced the presence of beneficial microbes in the rat model of streptozotocin-induced diabetes.

摘要

背景

肠道微生物群在众多生物学功能中起着关键作用,并且已成为糖尿病发展的驱动力。饮食有助于肠道微生物群的多样性和功能,为该疾病的预防和管理提供了一种手段。本研究旨在调查用开心果进行饮食干预对1型糖尿病大鼠模型肠道微生物群组成的影响,开心果是单不饱和脂肪酸、膳食纤维和植物化学物质的丰富来源。

方法

将雄性Wistar大鼠随机分为四组:接受对照饮食(CD)或开心果饮食(PD)的健康动物,以及接受对照饮食(DCD)或开心果饮食(DPD)4周的糖尿病动物。在饮食干预结束时测定血浆生化参数,并对肝脏和胰腺进行组织学检查。分析空肠、回肠、盲肠和结肠中附着的肠道微生物群。通过微生物分析和16S rRNA测序确定研究开始和结束时的粪便微生物群。

结果

两组糖尿病动物均表现出血浆葡萄糖水平高和胰岛素浓度低,以及特征性胰腺病变。补充开心果显著增加了空肠、回肠和盲肠中的乳酸杆菌和双歧杆菌数量(P<0.05),并使糖尿病动物所有检查肠道区域的微生物群正常化。补充4周后,健康和糖尿病动物粪便中的双歧杆菌和乳酸杆菌数量均增加,而肠球菌水平降低(P<0.05)。粪便样本的下一代测序显示,接受开心果饮食的健康动物中,分别增加和减少。糖尿病动物中的操作分类单元(OTUs)更高,并且在开心果治疗组中随时间增加,同时在给予开心果的健康动物中,、和种群的丰度增加。值得注意的是,健康大鼠中 的相对丰度高于糖尿病大鼠(P<0.05)。

结论

在链脲佐菌素诱导的糖尿病大鼠模型中,食用开心果可恢复正常菌群并增加有益微生物的数量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/5f37fea1aa00/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/af3b99584071/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/809e79da2259/gr2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/7c3d1052bd47/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/64997a91c666/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/391e098ade7d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/5f37fea1aa00/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/af3b99584071/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/809e79da2259/gr2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/7c3d1052bd47/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/64997a91c666/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/391e098ade7d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/371c/7424811/5f37fea1aa00/gr6.jpg

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