1651-P: Fermented Adlay Bran Extract Delays Early Postprandial Dysglycemia via Gut Motility Modulation Independent of Insulin Secretion

Introduction and Objective: Early postprandial dysglycemia precedes fasting hyperglycemia and contributes to metabolic deterioration. Most glucose-lowering strategies target insulin secretion or peripheral insulin sensitivity, whereas gastrointestinal approaches have focused on enzymatic inhibition or incretin signaling, with limited attention to glucose entry timing. We examined whether fermented adlay bran extract improves early postprandial glucose control via gut motility modulation independent of insulin secretion. Methods: We evaluated the metabolic effects of a fermented adlay bran extract (FRA), generated by fermentation of adlay bran residues remaining after ethanol extraction as a secondary use of an agricultural by-product, in mouse models of early dysglycemia. Oral and intraperitoneal glucose tolerance tests were performed to distinguish gut-dependent from systemic glucose handling. Gastric emptying was assessed using a phenol red assay. Intestinal transcriptomic analysis identified pathways related to gut motility. Fasting serum insulin levels were measured. Results: FRA attenuated postprandial glucose excursions during oral glucose tolerance testing and reduced fasting glucose levels without changes in body weight or adiposity. No effect was observed during intraperitoneal glucose tolerance testing, and fasting serum insulin levels remained unchanged. FRA delayed gastric emptying and downregulated intestinal smooth muscle-associated gene expression, consistent with delayed glucose entry during the early postprandial phase. These effects were characterized by a delayed and more gradual rise in postprandial glucose levels. Conclusion: Fermented adlay bran extract improves postprandial and fasting glycemia through modulation of gastric emptying and intestinal motility without increasing insulin secretion, suggesting a gut-based, weight-independent mechanism for early glycemic control. Disclosure J. Van: None. Y. Seong: None. H. Jeong: None. C. Choi: None. B. Lee: None. Funding This work was supported by the Global Joint Research Program funded by the Pukyong National University (2025).This research was also supported by Gyeonggido Business & Science Accelerator (GBSA) grant funded by the Gyeonggi provincial government.