Human gut microbiota transferred to germ-free NOD mice modulate the progression towards type 1 diabetes regardless of the pace of beta cell function loss in the donor

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388971%3A_____%2F19%3A00510175" target="_blank" >RIV/61388971:_____/19:00510175 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/19:10394981 RIV/00064203:_____/19:10394981

Výsledek na webu

<a href="https://link.springer.com/article/10.1007%2Fs00125-019-4869-2" target="_blank" >https://link.springer.com/article/10.1007%2Fs00125-019-4869-2</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s00125-019-4869-2" target="_blank" >10.1007/s00125-019-4869-2</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Human gut microbiota transferred to germ-free NOD mice modulate the progression towards type 1 diabetes regardless of the pace of beta cell function loss in the donor

Popis výsledku v původním jazyce

Aims/hypothesis This study aimed to assess the ability of human gut microbiota to delay the onset of type 1 diabetes when transferred into germ-free NOD mice.nMethods Two children with rapid and three children with slow beta cell function loss (as assessed by C-peptide AUC change in the mixed-meal tolerance tests performed 1 and 12 months after type 1 diabetes onset), participating in an ongoing trial with gluten-free diet, donated faeces, which were transferred into germ-free NOD mice. The mice were subsequently followed for diabetes incidence.nResults The bacterial profiles of bacteriome-humanised mice had significantly (p < 10(-5)) lower alpha diversity than the donor material, with marked shifts in ratios between the main phyla. Diabetes onset was significantly delayed in all bacteriome-humanised colonies vs germ-free NOD mice, but the pace of beta cell loss was not transferable to the mouse model.nConclusions/interpretation Germ-free NOD mice colonised with human gut microbiome are able to adopt a large proportion of transferred bacterial content, although the ratios of main phyla are reproduced only suboptimally. The recipient mice did not replicate the phenotype of the stool donor in relation to the pace towards type 1 diabetes.

Název v anglickém jazyce

Human gut microbiota transferred to germ-free NOD mice modulate the progression towards type 1 diabetes regardless of the pace of beta cell function loss in the donor

Popis výsledku anglicky

Aims/hypothesis This study aimed to assess the ability of human gut microbiota to delay the onset of type 1 diabetes when transferred into germ-free NOD mice.nMethods Two children with rapid and three children with slow beta cell function loss (as assessed by C-peptide AUC change in the mixed-meal tolerance tests performed 1 and 12 months after type 1 diabetes onset), participating in an ongoing trial with gluten-free diet, donated faeces, which were transferred into germ-free NOD mice. The mice were subsequently followed for diabetes incidence.nResults The bacterial profiles of bacteriome-humanised mice had significantly (p < 10(-5)) lower alpha diversity than the donor material, with marked shifts in ratios between the main phyla. Diabetes onset was significantly delayed in all bacteriome-humanised colonies vs germ-free NOD mice, but the pace of beta cell loss was not transferable to the mouse model.nConclusions/interpretation Germ-free NOD mice colonised with human gut microbiome are able to adopt a large proportion of transferred bacterial content, although the ratios of main phyla are reproduced only suboptimally. The recipient mice did not replicate the phenotype of the stool donor in relation to the pace towards type 1 diabetes.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10606 - Microbiology

Projekt

<a href="/cs/project/NV16-27994A" target="_blank" >NV16-27994A: Vliv bezlepkové diety na reziduální kapacitu beta buněk, imunitní funkce a střevní mikrobiom u dětí s nově manifestovaným diabetem 1. typu</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Diabetologia

ISSN

0012-186X

e-ISSN

—

Svazek periodika

62

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

6

Strana od-do

1291-1296

Kód UT WoS článku

000471176200019

EID výsledku v databázi Scopus

2-s2.0-85065042286