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Anti-obesity refers to a broad therapeutic category and a clinical objective focused on reducing excess body fat and managing the metabolic complications associated with obesity and overweight [1, 2]. It is not a single molecular target or receptor but rather a pharmacological designation for agents that influence energy homeostasis through a variety of central and peripheral pathways [3, 5]. Key molecular targets within this landscape include the Glucagon-like peptide 1 receptor (GLP-1R), the Glucose-dependent insulinotropic polypeptide receptor (GIPR), and the Melanocortin 4 receptor (MC4R), all of which play critical roles in central appetite regulation and satiety signaling within the hypothalamus [2, 4, 6]. Additionally, peripheral targets such as pancreatic and gastric lipases are utilized to decrease the digestion and absorption of dietary lipids, while monoamine transporters are modulated to affect neurotransmitters like norepinephrine and serotonin to suppress hunger [1, 3, 7]. Modern anti-obesity research has shifted toward potent peptide analogs and multi-target agonists that mimic endogenous metabolic hormones to achieve synergistic weight loss and improvements in metabolic health markers [4, 12]. These pharmacological interventions are essential for addressing the global obesity epidemic and mitigating the risk of associated chronic conditions, including type 2 diabetes, hypertension, and cardiovascular disease [4, 8].
Anti-obesity pharmacotherapy operates through several distinct mechanisms: the agonism of incretin receptors (GLP-1R and GIPR) to enhance satiety and delay gastric emptying; the activation of MC4 receptors in the central nervous system to reduce food intake; the inhibition of gastrointestinal lipases to prevent the absorption of dietary fats; and the modulation of monoamine reuptake (serotonin, norepinephrine, and dopamine) to suppress appetite and reduce food cravings [1, 2, 3, 5, 6, 12].
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