The management of postprandial glucose excursions in type 1 diabetes has a major impact on overall glycaemic control. In this work, we propose and evaluate various mechanistic models to characterize the disposal of meal-attributable glucose. Sixteen young volunteers with type 1 diabetes were subject to a variable-target clamp which replicated glucose profiles observed after a highglycaemic-load (n = 8) or a low-glycaemic-load (n = 8) evening meal. [6,6-2 H 2 ] and [U-13 C;1,2,3,4,5,6,6-2 H 7 ] glucose tracers were infused to, respectively, mimic: (a) the expected post-meal suppression of endogenous glucose production and (b) the appearance of glucose due to a standard meal. Six compartmental models (all a priori identifiable) were proposed to investigate the remote effect of circulating plasma insulin on the disposal of those glucose tracers from the non-accessible compartments, representing e.g. interstitium. An iterative population-based parameter fitting was employed. Models were evaluated attending to physiological plausibility, posterior identifiability of their parameter estimates, accuracy-via weighted fitting residuals-and information criteria (i.e. parsimony). The most plausible model, best representing our experimental data, comprised: (1) a remote effect x of insulin active above a threshold x c = 1.74 (0.81-2.50) • 10~2 min -1 [median (inter-quartile range)], with parameter XQ having a satisfactory support: coefficient of variation CV = 42.33 (31.34-65.34) %, and (2) steady-state conditions at the onset of the experiment (t = 0) for the compartment representing the remote effect, but not for the masses of the tracer that mimicked endogenous glucose production. Consequently, our mechanistic model suggests non-homogeneous changes in the disposal rates for meal-attributable glucose in relation to plasma insulin. The model can be applied to the in silico simulation of meals for the optimization of postprandial insulin infusion regimes in type 1 diabetes.