10 T1DM patients and 10 healthy age gender and BMI matched control subjects will be recruited. Patients will be on their usual insulin pump therapy, and the rate of the basal insulinization will be kept constant from 02:00 AM until the end of studies. All subjects will be studied on 3 separate occasions at 1-2 weeks intervals. In patients, study 1 will be a standard 120 min euglycemic insulin clamp. Timed blood samples will be collected to measure insulin levels at 10'-30' intervals. Plasma glucose will be measured at bedside by a YSI Glucose Analyzer; subcutaneous glucose will be monitored by CGM. In controls, study 1 will be a frequently sampled IVGTT of 240 min of duration. Timed blood samples (n=27) for glucose, C-peptide and insulin will be collected. Studies 2 and 3 will be identical in both patients and controls. They will be performed in randomized order and will last 360'. After a 60 min baseline period, at time 0' subjects will ingest either a 320 kcal (study 2) or a 640 kcal (study 3) meal. Meal composition (%Kcal: 53.3% carbohydrate, 28.2% lipid, 18.5% protein) will be Indian corn polenta plus parmesan cheese. Patients will program their pump to inject at time 0' a meal insulin bolus dose, calculated as usual. Blood samples (n=20) will be collected at timed intervals to measure plasma glucose, 13C/12C-glucose ratio, insulin, glucagon and C-peptide (the latter one only in control subjects). At a lower time frequency, triglycerides, non-esterified fatty acids (NEFA), active glucagon-like peptide-1 (GLP1) and total gastric inhibitory peptide (GIP) will also be measured. Subcutaneous glucose will be monitored by CGM only in patients. Data derived from IVGTT in controls will take the role played by the insulin clamp data in T1DM patients. Past experiments and also unpublished observations in our laboratory have shown that similar values of insulin sensitivity are obtained with IVGTT and insulin clamps in healthy people. The other difference is that, instead of the insulin pump, a beta cell secretion minimal model will be used, as previously described. The availability of 12C/13C-glucose ratio determinations will enrich further this picture, allowing to compute the contribution of meal carbohydrate to total plasma glucose and, by difference, the contribution of endogenous (primarily liver) production to total glucose. This data enrichment will result into further model development at step 3 (in both controls and patients) and will allow to split total insulin action into its two components, the one acting on endogenous glucose production and the one acting on glucose utilization. The former will be relevant to interpret the glucagon and, possibly, also the active GLP1 data.