Sugar may cause metabolic disorders by triggering microbiome imbalance, scientists flag

30 Aug 2022 --- A team of researchers has found that sugar alters the gut microbiota, which in turn causes weight gain and, potentially, pre-diabetes in mice. The Columbia University (US) study suggests that a balanced diet and healthy microbiome may be the key to preventing metabolic disorders such as diabetes and obesity.

Though it is known that the typical Western high in sugar, salt and fat (HFSS) diet can cause metabolic syndromes, the mechanisms by which unhealthy diets “kickstart” these changes were previously unknown.

“Our study emphasizes that a complex interaction between diet, microbiota, and the immune system plays a key role in the development of obesity, metabolic syndrome, type 2 diabetes, and other conditions,” says Dr. Ivalyo Ivanov, professor of microbiology & immunology at Columbia University and lead author of the study. 

“It suggests that for optimal health, it is important not only to modify your diet but also improve your microbiome or intestinal immune system, for example, by increasing Th17 cell-inducing bacteria,” he explains.

Critical shifts in microbiomeThe study shows that sugar may have more of an influence on metabolic diseases than fat.
The researchers fed a typical HFSS Western diet to mice for four weeks and tested the makeup of the mice’s microbiome throughout the duration. 

By the end of the four weeks, the animals were found to have glucose intolerance, insulin resistance and weight gain – all signs of pre-diabetes. 

Moreover, the rodents’ microbiomes changed. The segmented-filamentous bacteria common in chicken, fish and rodents had decreased significantly according to the study published in Cell. The effect was the animals’ Th17 immune cells in the microbiome also dropped significantly. Further experimentation showed that these Th17 immune cells play a prominent role in preventing metabolic syndromes.

“Microbiota are important, but the real protection comes from the Th17 cells induced by the bacteria,” underscores Ivanov. “These immune cells produce molecules that slow down the absorption of ‘bad’ lipids from the intestines, and they decrease intestinal inflammation.” 

“In other words, they keep the gut healthy and protect the body from absorbing pathogenic lipids.”

Of mice and menThe research shows that supplementing immune cells may help fight diseases like diabetes and obesity.
Though humans do not have segmented-filamentous bacteria, nor the Faecalibaculum rodentium that replaced them in the rodent microbiome, the researchers believe that similar bacteria in humans may respond to sugar in the same way. The study further revealed within the HFSS diet, sugar was the main culprit as it reduced Th17 bacteria and increased others. 

“Sugar eliminates the filamentous bacteria, and the protective Th17 cells disappear as a consequence,” Ivanov stresses. “When we fed mice a sugar-free, high-fat diet, they retained the intestinal Th17 cells and were completely protected from developing obesity and pre-diabetes, even though they ate the same number of calories.”

Additionally, the study notes that merely eliminating sugar did not alleviate the problem for all of the mice. For instance, mice already lacking in Th17 still developed obesity and diabetes. 

However, the study also found that giving supplements of immunity-producing bacteria led to more Th17 and less obesity and pre-diabetes despite still receiving a high-fat diet. 

Ivanov elaborates: “This suggests that some popular dietary interventions, such as minimizing sugars, may only work in people who have certain bacterial populations within their microbiota.”

He notes that supplementing Th17 cells may be therapeutic for people and mice, yet further study is needed.

Edited by William Bradford Nichols

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