Title of Study: “Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome”

Published: 29th August, 2022 | Authors: Yoshinaga Kawano, Madeline Edwards, Yiming Huang, Daniel Mucida, Kenya Honda, Ivaylo I. Ivanov | 🔗 View study here

Note: This study was performed on mice not humans.

Fundamental Findings:

Microbiota (gut bacteria) help control our body’s health, but we don’t fully understand how.

This study found that some microbes in the gut can protect us from getting fat and developing other health problems.

These good microbes help us by making special cells called Th17 cells.

When we have a diet with too much fat and sugar, we lose these beneficial microbes and Th17 cells.

This makes it easier for us to develop health problems. But bring them back and our body is protected again.

The Th17 cells help control how our body absorbs fat from the food we eat.

The negative effects of a high-fat diet happen because of the sugar in the diet. When we remove sugar from a high-fat diet, our body stays healthier, and the Th17 cells can protect us.

Sugar in our diet also helps harmful bacteria grow in our gut, which makes it harder for the beneficial bacteria to protect us.

The study helps us understand how our diet, gut microbes, and our body’s defense system works together to keep us healthy.

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.”

Graphical Abstract: