Sugar Changes The Microbiome

Researchers from Columbia University Vagelos College of Physicians and Surgeons set out to investigate the impact of the typical Western-style diet of the microbiome on mice.

In the four-week study, scientists found that the mice showed signs of metabolic syndrome, including weight gain, glucose intolerance, and insulin resistance. Moreover, the animals’s microbiomes were altered — segmented filamentous bacteria (found in rodents, fish, and chickens) decreased and other bacteria increased significantly.

Turns out, a drop in filamentous bacteria negatively effects Th17 immune cells, which are essential for preventing metabolic disease, diabetes, and weight gain. A decrease in filamentous bacteria was associated with fewer Th17 cells in the gut.

“These immune cells produce molecules that slow down the absorption of ‘bad’ lipids from the intestines and they decrease intestinal inflammation,” says lead researcher Ivalyo Ivanov, PhD. “In other words, they keep the gut healthy and protect the body from absorbing pathogenic lipids.”

Are fat and sugar both to blame?It doesn’t appear that way, say the researchers.

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

The research team also observed that while diet definitely matters, having a healthy, balanced gut is equally important. More research is needed to fully understand how diet triggers microbiome changes.

In Summary
How intestinal microbes regulate metabolic syndrome is incompletely understood. We show that intestinal microbiota protects against development of obesity, metabolic syndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells.

High-fat, high-sugar diet promoted metabolic disease by depleting Th17-inducing microbes, and recovery of commensal Th17 cells restored protection.

Microbiota-induced Th17 cells afforded protection by regulating lipid absorption across intestinal epithelium in an IL-17-dependent manner. Diet-induced loss of protective Th17 cells was mediated by the presence of sugar.

Eliminating sugar from high-fat diets protected mice from obesity and metabolic syndrome in a manner dependent on commensal-specific Th17 cells.

Sugar and ILC3 promoted outgrowth of Faecalibaculum rodentium that displaced Th17-inducing microbiota. These results define dietary and microbiota factors posing risk for metabolic syndrome.

They also define a microbiota-dependent mechanism for immuno-pathogenicity of dietary sugar and highlight an elaborate interaction between diet, microbiota, and intestinal immunity in regulation of metabolic disorders.