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2017 ; 6
(9
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Gut Microbiota-Dependent Trimethylamine-N-oxide and Serum Biomarkers in Patients
with T2DM and Advanced CKD
#MMPMID28925931
Al-Obaide MAI
; Singh R
; Datta P
; Rewers-Felkins KA
; Salguero MV
; Al-Obaidi I
; Kottapalli KR
; Vasylyeva TL
J Clin Med
2017[Sep]; 6
(9
): ä PMID28925931
show ga
Trimethylamine-N-oxide (TMAO) is a product of dietary, gut microbiome, and
tissues metabolism. Elevated blood TMAO levels are associated with heart attack,
stroke and chronic kidney disease (CKD). The purpose of our study was to
investigate the gut microbiota associated with trimethylamine (TMA) production,
the precursor of TMAO, and the serum levels of TMAO and inflammatory biomarkers
associated with type 2 diabetes mellitus (T2DM) and CKD. Twenty adults with T2DM
and advanced CKD and 20 healthy adults participated in the study. Analyses
included anthropometric and metabolic parameters, characterization of TMA
producing gut microbiota, and concentrations of TMAO, lipopolysaccharides (LPS)
endotoxin, zonulin (Zo) gut permeability marker, and serum inflammatory and
endothelial dysfunction biomarkers. Diversity of the gut microbiota was
identified by amplification of V3-V4 regions of the 16S ribosomal RNA genes and
DNA sequencing. TMAO was quantified by Mass Spectrometry and serum biomarkers by
ELISA. The significance of measurements justified by statistical analysis. The
gut microbiome in T2DM-CKD patients exhibited a higher incidence of TMA-producing
bacteria than control, p < 0.05. The serum levels of TMAO in T2DM-CKD patients
were significantly higher than controls, p < 0.05. TMAO showed a positive
correlation with Zo and LPS, inflammatory and endothelial dysfunction biomarkers.
A positive correlation was observed between Zo and LPS in T2DM-CKD subjects. An
increased abundance of TMA-producing bacteria in the gut microbiota of T2DM-CKD
patients together with excessive TMAO and increased gut permeability might impact
their risk for cardiovascular disease through elevation of chronic inflammation
and endothelial dysfunction.