A portion of absorbed dietary triglycerides (TG) is retained in the intestine after the postprandial period, within intracellular and extracellular compartments. This pool of TG can be mobilized in response to several stimuli, including oral glucose. The objective of this study was to determine whether oral glucose must be absorbed and metabolised in order to mobilize TG in rats, and whether high fat feeding, a model of insulin resistance, alters the lipid mobilization response to glucose. Lymph flow, TG concentration, TG output, apolipoprotein B48 (apoB48) concentration and output were assessed after an intraduodenal (i.d.) lipid bolus in rats exposed to the following i.d. administrations 5 hours later: saline (placebo), glucose, 2-deoxyglucose (2-DG, absorbed but not metabolised) or glucose + phlorizin (intestinal glucose absorption inhibitor). Glucose alone but not 2-DG or glucose + phlorizin treatments stimulated lymph flow, TG output and apoB48 output compared to placebo. The effects of glucose in high fat fed rats was similar to chow fed rats. In conclusion, glucose must be both absorbed and metabolized to enhance lymph flow and intestinal lipid mobilization. This effect is qualitatively and quantitatively similar in high fat and chow fed rats. The precise signaling mechanism whereby enteral glucose enhances lymph flow and mobilizes enteral lipid remains to be determined.