The mysterious role of the microorganisms in the human intestine has become increasingly compelling, with research demonstrating that these microbes can regulate metabolic diseases. New research published in Cell points to intestinal microbiota possibly protecting against the development of prediabetes and explains why high-sugar diets can deplete the supply of these “good microbes.”

Ivalyo Ivanov, PhD, associate professor of microbiology and immunology at Columbia University Vagelos College of Physicians and Surgeons, and colleagues embarked on a scientific journey to explore the changes in the gut microbiome that occur when subjects were fed a high-sugar and high-fat diet. Although the aspect of excessive calories contributing to obesity and diabetes has long been established, this team hypothesized that there was more to the story.

The researchers wrote that although they recognized the mechanism of this metabolic regulation is widely still unknown, their research showed “that intestinal microbiota protects against development of obesity, metabolic syndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells.” Microbiota-induced Th17 cells exhibited protective processes, which included regulation of lipid absorption that occurs across intestinal epithelium in an IL-17-dependent manner, and loss of protective Th17 cells was mediated by the presence of sugar in the diet.

“Sugar eliminates the filamentous bacteria, and the protective Th17 cells disappear as a consequence,” stated Dr. Ivanov. “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.”

Dr. Ivanov added, “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.”

However, eliminating sugar did not help all of the mice. Among mice lacking any filamentous bacteria to begin with, elimination of sugar did not have a beneficial effect, and the animals became obese and developed diabetes.

In response to the findings, Dr. Ivanov commented, “This suggests that some popular dietary interventions, such as minimizing sugars, may only work in people who have certain bacterial populations within their microbiota. 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,” adding, “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.”

The authors 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.

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