The clinical utilization of Tesofensine, a triple monoamine reuptake inhibitor, to exert favorable effects on metabolic health, primarily through appetite suppression and the enhancement of energy expenditure. Its mechanism of action influences central nervous system pathways that regulate satiety and thermogenesis, leading to a clinically significant reduction in visceral adipose tissue and improved body composition metrics. This support is a pharmacological tool for advanced weight and metabolic management.
Origin
Tesofensine was originally developed for the treatment of Alzheimer’s disease, but clinical trials revealed its potent and consistent effect on weight loss, shifting its primary focus to metabolic and obesity management. The concept of “Metabolic Support” acknowledges its role in facilitating the difficult process of sustained caloric deficit and metabolic recalibration. Its application is based on neuropharmacological modulation of energy balance.
Mechanism
Tesofensine operates by inhibiting the reuptake of norepinephrine, dopamine, and serotonin in the synaptic cleft, increasing the concentration of these neurotransmitters in the brain. The elevated levels of norepinephrine and dopamine stimulate the central satiety centers in the hypothalamus, reducing hunger and increasing the feeling of fullness. Furthermore, the sympathetic activation can lead to increased resting energy expenditure, collectively supporting a negative energy balance and improving overall metabolic function.
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