Posted on: Friday, January 6th 2017 (and 2014) at 7:15 pm
Written By:Sayer Ji, Founder
A groundbreaking new study published in the prestigious journal
Nature has revealed how non-caloric artificial sweeteners (NAS) drive obesity-
and diabetes-related changes in both mice and humans.
The study titled, "Artificial sweeteners induce glucose intolerance by
altering the gut microbiota," states:
"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."
Part 1: Gut Bacteria Mediate Artificial Sweetener-Induced Blood
Sugar Disturbances
The researchers administered commercially available formulations
of saccharin (Sweet' N Low), sucralose (Splenda) or aspartame (Equal) in the
drinking water of 10-week old mice. The control group received I either glucose
or sucrose. After 11 weeks, the three artificial sweetener fed groups developed
"marked glucose intolerance," with saccharin having the most
deleterious effects followed by sucralose and aspartame.
Graph showing the effects of artificial
sweeteners on blood glucose levels.
The researchers hypothesized that since artificial sweeteners
pass through the gut mostly unabsorbed by the body that the microbiota may be
responsible for regulating their observed adverse effects on blood sugar.
To test their theory they administered antibiotics to mice while keeping them
on their diet and sweetener supplementation regimens. Their results indicate
that gut bacteria indeed drive the adverse effects of these sweeteners:
"Notably, after 4 weeks of antibiotic treatment, differences
in glucose intolerance between NAS-drinking mice and controls were abolished
both in the lean and the obese states. Similar effects were observed with the
Gram-positive-targeting antibiotic vancomycin ('antibiotics B',
0.5 g l−1). These results suggest that NAS-induced glucose
intolerance is mediated through alterations to the commensal microbiota, with
contributions from diverse bacterial taxa."
Finally, in order to test whether the role of microbiota in
upsetting blood sugar balance was 'cause and effect' they performed a fecal
transplant from mice receiving saccharin or glucose into germ-free mice
receiving the same normal-chow diet. Their results confirmed the crucial
role of the microbiota in inducing blood sugar disturbing effects:
"Notably, recipients of microbiota from mice consuming
commercial saccharin exhibited impaired glucose tolerance as compared to
control (glucose) microbiota recipients, determined 6 days following
transfer. Transferring the microbiota composition of HFD-consuming mice
drinking water or pure saccharin replicated the glucose intolerance phenotype.
Together, these results establish that the metabolic derangements induced by
NAS consumption are mediated by the intestinal microbiota."
