Sugar Disrupts Microbiome, Eliminates Protection Against Obesity and Diabetes


A study in mice found that dietary sugar alters the gut microbiome, setting off a chain of events that leads to metabolic disease, prediabetes and weight gain.

The findings, published today in Cell, suggest that diet is important, but an optimal microbiome is equally important for the prevention of metabolic syndrome, diabetes and obesity.

Diet changes the microbiome

A Western-style high-fat, high-sugar diet can lead to obesity, metabolic syndrome and diabetes, but it’s unclear how the diet triggers unhealthy changes in the body.

The gut microbiome is critical to an animal’s nutrition, which is why Ivalyo Ivanov, Ph.D., associate professor of microbiology and immunology at Columbia University Vagelos College of Physicians and Surgeons, and colleagues studied the initial effects of the western diet on the microbiota of mice.

After four weeks on the diet, the animals exhibited the hallmarks of the metabolic syndrome, such as weight gain, insulin resistance, and glucose intolerance. And their microbiomes had changed dramatically, with the amount of segmented filamentous bacteria — common in the gut microbiota of rodents, fish, and chickens — dropping sharply and other bacteria increasing in abundance.

Microbiome changes alter Th17 cells

Reducing filamentous bacteria, the researchers found, was critical to animal health through its effect on Th17 immune cells. The decline in filamentous bacteria reduced the number of Th17 cells in the intestine, and further experiments revealed that it is Th17 cells that are needed to prevent metabolic disease, diabetes and weight gain.

“These immune cells produce molecules that slow the absorption of ‘bad’ lipids from the intestines and decrease intestinal inflammation,” says Ivanov. “In other words, they keep the intestine healthy and protect the body against the absorption of pathogenic lipids.”

Sugar vs Fat

What component of the high-fat, high-sugar diet led to these changes? Ivanov’s team found that the sugar was to blame.

“The sugar eliminates the filamentous bacteria and the protective Th17 cells disappear as a result,” says Ivanov. “When we fed mice a sugar-free, high-fat diet, they retained intestinal Th17 cells and were completely protected against the development of obesity and prediabetes, even though they ate the same number of calories. “

But eliminating the sugar didn’t help all the mice. Among those initially lacking filamentous bacteria, sugar removal had no beneficial effect, and the animals became obese and developed diabetes.

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

In these cases, some probiotics might be helpful. In Ivanov’s mice, supplements of filamentous bacteria led to salvage of Th17 cells and protection against metabolic syndrome, despite the animals consuming a high-fat diet.

Although people don’t have the same filamentous bacteria as mice, Ivanov thinks other bacteria in humans may have the same protective effects.

Providing Th17 cells to mice also provided protection and may also be therapeutic for humans. “The microbiota is important, but the real protection comes from the bacteria-induced Th17 cells,” says Ivanov.

“Our study highlights that a complex interplay 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 Ivanov. . “This suggests that for optimal health, it is important not only to modify your diet, but also to improve your gut microbiome or immune system, for example by increasing bacteria inducing Th17 cells.”


Comments are closed.