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Signalling cascade after agonist binding to GLP-1R (in vitro / in vivo animal model): Activation of the Gs protein leads to stimulation of adenylate cyclase, an increase in cAMP concentration, and activation of PKA and Epac2 In pancreatic -cells: the rise in cAMP leads to glucose-dependent insulin secretion an important distinction from sulfonylureas, which stimulate secretion independently of glucose concentration In POMC neurons of the hypothalamic arcuate nucleus: GLP-1R activation induces the release of -MSH onto MC4R receptors in the paraventricular nucleus satiety signalling and inhibition of food intake In NTS neurons of the brainstem: GLP-1R activation modulates afferent signalling from the vagus nerve slowing of gastric emptying In the mesolimbic circuit (ventral tegmental area, nucleus accumbens): modulation of dopaminergic signalling in response to caloric stimuli this is the mechanism underlying the observed reduction in preference for high-calorie foods in behavioural models In DIO mouse models (diet-induced obesity, C57BL/6J) chronic exposure to semaglutide (usually 1060 nmol/kg s.c., once every 23 days) led to a 1015% reduction in body weight relative to the control group over 46 weeks