What is it about?

The human intestine is home to a vast number of bacteria, and the intestinal barrier prevents under physiological conditions, the passage of harmful luminal contents such as lipopolysaccharide (LPS). Type 2 diabetes is associated with changes in gut microbiota and impaired intestinal barrier functions, leading to translocation of microbiota-derived LPS into the circulatory system, a condition referred to as metabolic endotoxemia. We investigated the effects of metabolic endotoxemia after experimental stroke in a murine model of type 2 diabetes.

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Why is it important?

Diabetic mice exhibited metabolic endotoxemia (an altered gut microbial composition, increased intestinal permeability, and higher plasma LPS levels), which was negatively associated with stroke outcomes. Moreover, gut microbiota modulation with a non-absorbable antibiotic attenuated LPS levels in the circulation, thereby in the ischemic brain and improved the stroke outcome. Our findings suggests that targeting metabolic endotoxemia might be a novel potential therapeutic strategy to improve stroke outcomes.

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This page is a summary of: Metabolic endotoxemia promotes neuroinflammation after focal cerebral ischemia, Journal of Cerebral Blood Flow & Metabolism, January 2020, SAGE Publications,
DOI: 10.1177/0271678x19899577.
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