Abstract
<jats:p>Bariatric surgery has evolved over time through empirical success rather than intestinal mechanistic and physiologic clarity, framed by the concepts of gastric restriction and intestinal exclusion. Duodenal exclusion emerged as the dominant model explanation following the observation of rapid diabetes remission after bypass procedures, which led to the erroneous interpretation of anatomical exclusion as a metabolic necessity. Duodenal-preserving operations have demonstrated that exclusion of the proximal intestine is not required to achieve durable metabolic benefits. Advances in enteroendocrinology and bile acid physiology have clarified that the metabolic effects of bariatric surgery arise from the reorganization of nutrient flow, altered temporal exposure of the intestine to nutrients and bile acids, and coordinated modulation of incretin and gut–brain signaling. In light of this concept, duodenal exclusion is a sufficient but physiologically blunt means of intensifying distal gut stimulation, rather than a fundamental principle of metabolic efficacy. Transit bipartition embodies this conceptual maturation. By redistributing nutrient transit through dual pathways while preserving duodenal continuity, it enhances ileal signaling without abolishing proximal regulatory function. This approach dissociates metabolic efficacy from anatomical sacrifice and rebrands bariatric surgery as physiological modulation rather than intestinal ablation. The shift from duodenal exclusion to preservation illuminates a broader reorientation of metabolic surgery: from enforcing metabolic change through exclusion to orchestrating it through controlled nutrient flow and signaling balance.</jats:p>