Introduction: Obesity is associated with measurably attenuated postprandial incretin responses, characterized by blunted glucagon-like peptide-1 (GLP-1) secretion and functional resistance to glucose-dependent insulinotropic polypeptide (GIP) signaling. Whether this enteroendocrine dysregulation represents a primary pathophysiological defect anteceding adiposity or a secondary maladaptive consequence of chronic metabolic overload remains unresolved, with substantial implications for the conceptualization and treatment of obesity.  Objective: To critically evaluate and synthesize the available evidence regarding endogenous incretin insufficiency in obesity, determining whether this phenomenon constitutes a primary etiological defect or a state-dependent metabolic adaptation. Methods: A structured narrative review was conducted across PubMed/MEDLINE, Embase, Scopus, and Web of Science. Eligible studies encompassed human clinical trials, mechanistic investigations, and translational experimental models addressing endogenous incretin physiology, obesity-associated hormonal dysregulation, and incretin-based pharmacotherapy outcomes.  Results: Evidence consistently demonstrates stimulus-dependent impairment of GLP-1 secretion and functional GIP resistance, both partially reversible following weight loss. Pharmacological amplification via GLP-1 receptor agonists, dual incretin agonists, and amylin-based therapies yields robust efficacy, indicating biologically intact but functionally downregulated signaling pathways. A multi-hormonal insufficiency model, rather than isolated incretin deficiency, best accounts for the observed phenotype.  Conclusion: Endogenous incretin insufficiency in obesity reflects a state-dependent, adaptive dysregulation of a biologically intact enteroendocrine system, driven by chronic metabolic stress, rather than a primary etiological defect. Therapeutic strategies should prioritize restoration of integrated satiety signaling over isolated hormonal replacement.