Sucralose linked to metabolic syndrome

Consuming low-calorie sweeteners could promote metabolic syndrome and even predispose obese people to prediabetes and diabetes, according to George Washington University researchers. The study involved separate tests on human fat-derived stem cells and fat samples.

“Our stem cell-based studies indicate that low-calorie sweeteners promote additional fat accumulation within cells compared with cells not exposed to these substances, in a dose-dependent fashion—meaning that as the dose of sucralose is increased more cells showed increased fat droplet accumulation,” said Sabyasachi Sen, M.D., Associate Professor of Medicine at George Washington University in Washington, D.C. “This most likely occurs by increasing glucose entry into cells through increased activity of genes called glucose transporters.”

In fat samples collected from obese subjects that consumed low-calorie sweeteners, researchers found similar effects.

The findings especially impact individuals who are overweight, obese, prediabetic and diabetic since they have more insulin resistance and may have more glucose in the blood - their risk of getting a heart attack or stroke is higher.

Effects of low-calorie sweeteners

Researchers chose the popular low-calorie sweetener, sucralose, on stem cells—cells that could change into mature fat, muscle, cartilage or bone cells—taken from human fat tissue. The cells sat in Petri dishes for 12 days in media that promotes fat production, to mimic an environment that promotes obesity.

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. This led them to conduct another experiment where they analysed biopsy samples of abdominal fat obtained from 18 subjects who said they consumed low-calorie sweeteners (sucralose and a trace of aspartame, and/or acesulfame potassium).

Four of the subjects had healthy weight, and fourteen were obese. In the healthy weight subjects, the difference in gene expressions were not significant. However, in the subjects with obesity or overweight, the researchers noted significant 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.
Sen previously conducted the same study on a total of eight subjects with similar results. “Because we found the same results with the, larger sample size, we have much more confidence that low-calorie sweeteners are causing metabolic dysfunction,” Sen said.

In a new cell culture study, Sen found that sucralose appears to promote oxygen radical accumulation – a highly reactive particles that can cause disease and inflammation inside cells. These oxygen radicals interfere with cell activity and slow down metabolism, which promotes accumulation of fat in the cell. “This provides another explanation of how sucralose may interfere with metabolism,” he said.