What is it about?
In this manuscript, we administered sodium butyrate, a short-chain fatty acid, which is produced by gut microbiota on digestion of complex carbohydrates (like dietary fibers) to animal models of type-1 diabetes (T1D). Butyrate administration reduced the progression of hyperglycemia in diabetic NOD mice and delayed onset of diabetes in the early-intervention group with a reduction in insulitis. Butyrate administration increased regulatory T cells (Tregs) in the colon, mesenteric lymph nodes, Peyer’s patches, and its protective effects diminished upon depletion of Tregs. Our results thus suggest that early administration of butyrate can restore immunological tolerance during T1D via induction of Tregs capable of migration to the pancreas and pancreatic lymph nodes.
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Why is it important?
As a safe postbitoic approach, oral administration of sodium butyrate or diets rich in butyrate offers an attractive adjunct therapeutic option for subjects with a recent diagnosis of type-1 diabetes.
Perspectives
The study can be expanded further in human subjects for dose standardization and efficacy testing.
Prof NARESH SACHDEVA
Post Graduate Institute of Medical Education and Research
Read the Original
This page is a summary of: Butyrate induced Tregs are capable of migration from the GALT to the pancreas to restore immunological tolerance during type-1 diabetes, Scientific Reports, November 2020, Springer Science + Business Media,
DOI: 10.1038/s41598-020-76109-y.
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