This thesis investigates the role of the essential micronutrient zinc in regulating glycemic control under normal, metabolic, and inflammatory conditions, with a particular focus on intestinal glucose absorption. While zinc is traditionally recognized for its role in insulin synthesis and signaling, its influence on glucose homeostasis beyond pancreatic function, particularly within intestinal tissue, remains incompletely understood. Using preclinical mouse models, this work demonstrates that oral glucose administration induces rapid, tissue-specific redistribution of zinc, while zinc supplementation, in turn, reduces systemic glycemic response. Zinc supplementation significantly improved oral glucose tolerance independent of insulin action, an effect not observed with intraperitoneal glucose administration, indicating a primary role within the small intestine. Mechanistically, zinc reduced expression of key intestinal glucose transporters, Sglt1 and Glut2, and decreased epithelial glucose uptake in vivo and in vitro. Conversely, dietary- and genetic-induced zinc deficiency increased glycemic response and upregulated intestinal glucose transport pathways. Notably, increased expression of Sglt1 was observed in inflammation-induced zinc deficiency. However, zinc supplementation did not reduce glucose absorption nor expression of this transporter. Collectively, these findings identify the small intestine as a critical site of zinc-mediated glycemic regulation and establish zinc as a modulator of glucose absorption independent of insulin. This work provides mechanistic insight into inconsistent clinical outcomes and highlights zinc as a potential target for nutrition-based interventions in metabolic and inflammatory diseases.