By Chioma Umeha
Low-calorie, artificial sweeteners appear to play havoc with
the body’s metabolism, and large consumption of these sugar substitutes could
promote fat accumulation, especially in people who are already obese,
preliminary research suggests.
The study results will be presented Monday at ENDO 2017, the
Endocrine Society’s 99th annual meeting in Orlando, Fla.
“Many health-conscious individuals like to consume
low-calorie sweeteners as an alternative to sugar. However, there is increasing
scientific evidence that these sweeteners promote metabolic dysfunction,” said
Sabyasachi Sen, an Associate Professor of Medicine and Endocrinology at George
Washington University in Washington, D.C., and the study’s principal
investigator.
Sen and his colleagues tested sucralose, a popular
low-calorie sweetener, on stem cells- cells that could change into mature fat,
muscle, cartilage or bone cells – taken from human fat tissue. They placed
these cells in Petri dishes for 12 days in media that promotes fat production.
At a 0.2-millimolar sucralose dose similar to the concentration found in the
blood of people with high consumption of low-calorie sweeteners – equal to four
cans of diet soda per day – the researchers said they observed increased
expression of genes that are markers of fat production and inflammation. There
also was increased accumulation of fat droplets in cells, particularly at a
larger dose (1 millimolar), Sen reported.
With this evidence, the investigators then conducted a
separate experiment. They analyzed biopsy samples of abdominal fat obtained
from eight subjects who said they consumed low-calorie sweeteners (mainly
sucralose and a trace of aspartame, and/or acesulfame potassium). Four of the subjects
were healthy weight, and four were obese. According to Sen, they saw evidence
of increased glucose (sugar) transport into cells and overexpression of known
fat-producing genes, compared with fat biopsy samples from subjects who did not
consume low-calorie sweeteners.
Additionally, he noted that subjects who consumed
low-calorie sweeteners, which are several-fold sweeter than sugar, showed an
overexpression of sweet taste receptors in their fat tissue; this
overexpression was up to 2.5-fold higher than in subjects without history of
consumption of these sweeteners. Overexpression of sweet taste receptors in the
abdominal fat, he said, may play a role in allowing glucose to enter cells,
from which the body absorbs it into the bloodstream.
All these findings are signs of metabolic dysregulation in
which the cellular mechanisms are changing to make more fat, he explained. Of
concern, Sen said, these effects were most apparent in the obese individuals
who consumed low-calorie sweeteners, rather than individuals of normal weight.
He added that the observed increased uptake of glucose into the cells is also
concerning for consumers who have diabetes and prediabetes, “who already have
more sugar in their blood,” compared to their counterparts who do not have diabetes.
More studies are necessary in larger numbers of people with
diabetes and obesity to confirm these findings, he stressed.
“However, from our study,” Sen stated, “we believe that
low-calorie sweeteners promote additional fat formation by allowing more
glucose to enter the cells, and promotes inflammation, which may be more
detrimental in obese individuals.”
