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Artificial Sweeteners and the Gut

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So, it turns out that artificial sweeteners are really bad for the composition of the gut microbiome.


Physiol Behav. 2016 Oct 1;164(Pt B):488-493. doi: 10.1016/j.physbeh.2016.04.029. 
Epub 2016 Apr 15.
Reshaping the gut microbiota: Impact of low calorie sweeteners and the link to
insulin resistance?
Nettleton JE(1), Reimer RA(2), Shearer J(3).

Disruption in the gut microbiota is now recognized as an active contributor
towards the development of obesity and insulin resistance. This review considers 
one class of dietary additives known to influence the gut microbiota that may
predispose susceptible individuals to insulin resistance - the regular, long-term
consumption of low-dose, low calorie sweeteners. While the data are
controversial, mounting evidence suggests that low calorie sweeteners should not 
be dismissed as inert in the gut environment. Sucralose, aspartame and saccharin,
all widely used to reduce energy content in foods and beverages to promote
satiety and encourage weight loss, have been shown to disrupt the balance and
diversity of gut microbiota. Fecal transplant experiments, wherein microbiota
from low calorie sweetener consuming hosts are transferred into germ-free mice,
show that this disruption is transferable and results in impaired glucose
tolerance, a well-known risk factor towards the development of a number of
metabolic disease states. As our understanding of the importance of the gut
microbiota in metabolic health continues to grow, it will be increasingly
important to consider the impact of all dietary components, including low calorie
sweeteners, on gut microbiota and metabolic health.

Copyright © 2016 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.physbeh.2016.04.029 
PMID: 27090230  [Indexed for MEDLINE]


Nature. 2014 Oct 9;514(7521):181-6. doi: 10.1038/nature13793. Epub 2014 Sep 17.

Artificial sweeteners induce glucose intolerance by altering the gut microbiota.

Suez J(1), Korem T(2), Zeevi D(2), Zilberman-Schapira G(3), Thaiss CA(1), Maza
O(1), Israeli D(4), Zmora N(5), Gilad S(6), Weinberger A(7), Kuperman Y(8),
Harmelin A(8), Kolodkin-Gal I(9), Shapiro H(1), Halpern Z(10), Segal E(7), Elinav

Non-caloric artificial sweeteners (NAS) are among the most widely used food
additives worldwide, regularly consumed by lean and obese individuals alike. NAS 
consumption is considered safe and beneficial owing to their low caloric content,
yet supporting scientific data remain sparse and controversial. Here we
demonstrate that consumption of commonly used NAS formulations drives the
development of glucose intolerance through induction of compositional and
functional alterations to the intestinal microbiota. These NAS-mediated
deleterious metabolic effects are abrogated by antibiotic treatment, and are
fully transferrable to germ-free mice upon faecal transplantation of microbiota
configurations from NAS-consuming mice, or of microbiota anaerobically incubated 
in the presence of NAS. We identify NAS-altered microbial metabolic pathways that
are linked to host susceptibility to metabolic disease, and demonstrate similar
NAS-induced dysbiosis and glucose intolerance in healthy human subjects.
Collectively, our results link NAS consumption, dysbiosis and metabolic
abnormalities, thereby calling for a reassessment of massive NAS usage.

DOI: 10.1038/nature13793 
PMID: 25231862  [Indexed for MEDLINE]


Front Physiol. 2017 Jul 24;8:487. doi: 10.3389/fphys.2017.00487. eCollection

Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver
Inflammation in Mice.

Bian X(1), Chi L(2), Gao B(1), Tu P(2), Ru H(3), Lu K(2).

Sucralose is the most widely used artificial sweetener, and its health effects
have been highly debated over the years. In particular, previous studies have
shown that sucralose consumption can alter the gut microbiota. The gut microbiome
plays a key role in processes related to host health, such as food digestion and 
fermentation, immune cell development, and enteric nervous system regulation.
Inflammation is one of the most common effects associated with gut microbiome
dysbiosis, which has been linked to a series of human diseases, such as diabetes 
and obesity. The aim of this study was to investigate the structural and
functional effects of sucralose on the gut microbiota and associated inflammation
in the host. In this study, C57BL/6 male mice received sucralose in their
drinking water for 6 months. The difference in gut microbiota composition and
metabolites between control and sucralose-treated mice was determined using 16S
rRNA gene sequencing, functional gene enrichment analysis and metabolomics.
Inflammatory gene expression in tissues was analyzed by RT-PCR. Alterations in
bacterial genera showed that sucralose affects the gut microbiota and its
developmental dynamics. Enrichment of bacterial pro-inflammatory genes and
disruption in fecal metabolites suggest that 6-month sucralose consumption at the
human acceptable daily intake (ADI) may increase the risk of developing tissue
inflammation by disrupting the gut microbiota, which is supported by elevated
pro-inflammatory gene expression in the liver of sucralose-treated mice. Our
results highlight the role of sucralose-gut microbiome interaction in regulating 
host health-related processes, particularly chronic inflammation.

DOI: 10.3389/fphys.2017.00487 
PMCID: PMC5522834
PMID: 28790923 

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