A Kinetic Modelling Approach to Understand Delayed and Impaired Starch Digestion Post-Intestinal Surgery and Tissue Remodelling

Abstract

Intestinal surgery and tissue remodelling significantly alter the digestive-absorptive landscape of the gastrointestinal tract, often resulting in delayed and incomplete starch digestion. Surgical interventions, such as resection, bypass, or tissue reconstruction, reduce the effective mucosal surface area, enzyme contact time, and glucose transporter density, thereby impairing nutrient assimilation. The altered intestinal geometry and flow dynamics accelerate chyme transit and reduce exposure to pancreatic α-amylase, α-glucosidase, and other brush border enzymes, leading to a shift in starch hydrolysis kinetics and a decrease in postprandial glucose release. In this study, starch digestion kinetic model was developed to quantitatively predict these physiological alterations. This model integrates Michaelis-Menten enzyme kinetics, diffusion limited hydrolysis and intestinal transport parameters under variable intestinal lengths and flow conditions. By simulating post-surgical changes in enzyme localization, luminal mixing, delayed hydrolysis of starch and glucose transport via SGLT1 and GLUT2, the model captures the delay in maltose and glucose formation and the subsequent reduction in absorption efficiency. The MATLAB simulation results demonstrate that kinetic modelling can effectively describe the nonlinear digestion–absorption dynamics arising from anatomical and functional alterations in the intestine. This approach provides a predictive framework for understanding nutrient malabsorption after intestinal surgery and offers a valuable tool for designing personalized dietary and therapeutic interventions in post-surgical metabolic management. In future prospects, simulation outputs can be validated against in vitro digestion data using modified intestinal flow reactors to replicate post-surgical conditions.