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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2017 ; 12
(6
): e0178426
Nephropedia Template TP
gab.com Text
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English Wikipedia
The artificial sweetener acesulfame potassium affects the gut microbiome and body
weight gain in CD-1 mice
#MMPMID28594855
Bian X
; Chi L
; Gao B
; Tu P
; Ru H
; Lu K
PLoS One
2017[]; 12
(6
): e0178426
PMID28594855
show ga
Artificial sweeteners have been widely used in the modern diet, and their
observed effects on human health have been inconsistent, with both beneficial and
adverse outcomes reported. Obesity and type 2 diabetes have dramatically
increased in the U.S. and other countries over the last two decades. Numerous
studies have indicated an important role of the gut microbiome in body weight
control and glucose metabolism and regulation. Interestingly, the artificial
sweetener saccharin could alter gut microbiota and induce glucose intolerance,
raising questions about the contribution of artificial sweeteners to the global
epidemic of obesity and diabetes. Acesulfame-potassium (Ace-K), a FDA-approved
artificial sweetener, is commonly used, but its toxicity data reported to date
are considered inadequate. In particular, the functional impact of Ace-K on the
gut microbiome is largely unknown. In this study, we explored the effects of
Ace-K on the gut microbiome and the changes in fecal metabolic profiles using 16S
rRNA sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics. We
found that Ace-K consumption perturbed the gut microbiome of CD-1 mice after a
4-week treatment. The observed body weight gain, shifts in the gut bacterial
community composition, enrichment of functional bacterial genes related to energy
metabolism, and fecal metabolomic changes were highly gender-specific, with
differential effects observed for males and females. In particular, ace-K
increased body weight gain of male but not female mice. Collectively, our results
may provide a novel understanding of the interaction between artificial
sweeteners and the gut microbiome, as well as the potential role of this
interaction in the development of obesity and the associated chronic
inflammation.