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Other mechanisms underlying the effects of GLP-1 RAs on exercise capacity include improvements in myocardial energetics, enhanced endothelial function, reductions in systemic inflammation and oxidative stress and modulation of skeletal muscle metabolism
A landmark study published in Diabetes (Tolhurst et al., 2012) demonstrated that SCFAs stimulate GLP-1 secretion via the FFAR2 receptor, and that mice lacking this receptor showed significantly reduced SCFA-triggered GLP-1 release
Persistent activation of TRPM4 triggers necrotic cell death characterized by sodium overload
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