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When these compounds activate the GLP-1 receptor, they initiate a cascade of downstream physiological events: Glucose-Dependent Insulin Secretion: They stimulate the pancreatic beta cells to release insulin, but notably only when circulating glucose levels are elevated

The pelvic floor muscles support the urinary sphincter, so as the muscles grow weaker, the urethra loses its ability to hold in urine

The intention-to-treat analysis showed no dementia risk difference between GLP1 receptor agonist and DPP4 inhibitor initiation

Probably due to the lack of complementary interacting residues, superimposing GIP or GLP-1 to GCG bound to GCGR shows that the aligned peptides reduced favorable contacts with GCGR compared to GCG by removing one hydrogen bond (Y10 P (GCG)/Y10 P (GIP)/V16 P (GLP-1)-Q142 1.40b (GCGR)) and pi-pi stacking (Y13 P (GCG)/A13 P (GIP)/Y19 P (GLP-1)-Y138 1.36b (GCGR)) and by repulsing the interaction between Y1 P (GIP) and I235 3.40b (GCGR)

Emily Cooper, Mark Wright, and Andrea Taylor open the listener mailbag to answer real questions from around the world about metabolism, hormones, and GLP-1 therapy