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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

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]

Second, the principle of 'start low and go slow' is paramount

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