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Microbiota are a source of low-grade inflammation during obesity and contribute to insulin resistance and poor blood glucose control among other mechanisms in the progression of type 2 diabetes.1 Nearly all bacteria that reside within the host are found in the intestine, but it is not yet clear how microbiota are a source of inflammation in the circulation or metabolic tissues during obesity. A key knowledge gap is understanding how obesity or certain diets promote gut barrier dysfunction that allows increased permeability for bacteria or bacterial components that can engage immune response and promote inflammation-induced metabolic dysfunction. Metabolic endotoxaemia is the key example of a bacterial source of inflammation. Obesity or diet-induced increases in lipopolysaccharides (LPS or endotoxin), that escape the gut lumen, penetrate the intestinal barrier and enter into the host circulation, cells and tissues. This low-level increase in LPS activate toll-like receptor 4, increase inflammation in multiple cell types, and can initiate insulin resistance and dysglycaemia.2
The intestinal mucosal-epithelial barrier harbours many lines of defence to limit the penetration of bacterial components such as LPS. Gut microbiota can shape intestinal morphology and alter intestinal function such as glucose absorption.3 It was not clear how obesity or obesogenic diets engage microbiota to compromise intestinal barrier function. High-fat diet (HFD) feeding decreases the expression of tight junction protein, zona occludens-1 (ZO-1), which is associated with increased intestinal permeability.2 ZO-1 and occludin are decreased in the intestine of genetically obese mice …
Twitter @HanFang_Hannah, @SchertzerLab
Contributors HF, RRe-L and JDS wrote and edited the manuscript.
Funding This study was funded by the Institute of Nutrition, Metabolism and Diabetes (FDN-154295).
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.