Abstract

Research examining the mechanisms of metabolic and bariatric surgery is frequently restricted to small-animal models. These preclinical models have demonstrated numerous surgical effects and greatly advanced our understanding of the intestine as an endocrine organ—effects that would otherwise be nearly impossible to identify clinically with current methods [1–3]. Despite these advantages, preclinical models remain limited because of the plethora of differences between rodent and human physiology that affect not only the interpretation but also the potential translation of findings to humans.

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