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Utilizing zebrafish models, researchers have elucidated fundamental mechanisms governing islet development, \u03b2-cell dysfunction, and metabolic dysregulation. These experimental systems have significantly advanced our understanding of various diabetes subtypes, including type 1, type 2, gestational, and monogenic forms, while also facilitating mechanistic studies of diabetic complications such as retinopathy and nephropathy. Recent model refinements, particularly in simulating monogenic disorders and pregnancy-associated metabolic changes, promise to deepen our comprehension of disease pathophysiology and therapeutic interventions. Nevertheless, a persistent limitation lies in their incomplete recapitulation of human-specific physiological complexity and multi-organ metabolic interactions, factors that may influence translational applicability. 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