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While the compound's primary mechanism involves reducing food intake through enhanced satiety, evidence suggests it also modestly increases resting energy expenditure through stimulation of noradrenergic pathways

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Similar redistribution changes following KCl-stimulated transient synaptic excitation have also been observed for N-cadherins in the literature [95], suggesting that synaptic adhesion molecules undergo positional redistribution in response to changes in synaptic function, which has the potential to alter interactions between synaptic adhesion molecules [72]