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466 One study proposed a novel mechanism wherein postprandial GLP-1 release, under normal physiological conditions, inhibits the activity of chemosensory cells in the carotid body, thereby counteracting sympathetic excitability mediated by elevated blood glucose or insulin levels

Distinct pathophysiological processes contribute to the rewiring of specific metabolic pathways and the development of vulnerabilities

It is most often studied in animal models of tendon, gut, and vessel injury, and is not an FDA-approved drug

Magnesium treatment reversed these effects

The role for gut-associated bacteria in T1D development was further reinforced through antibiotic treatment that reduced disease symptoms in experimental models and promoted sterile pancreatic lymph nodes (Costa et al