Exercise (E) induced increase in glucose uptake (Rd) is offset by compensatory increase in endogenous glucose production (EGP) in health. To determine the extent to which this occurs in type 1 diabetes (T1D) and to assess the effects of hyperglycemia and hyperinsulinemia, we studied six T1D subjects (age 29±7 years, BMI 28.3±4.8 kg/m2, VO2 max 28.7±10 ml/kg/min) on three visits (V1: euglycemia, low insulin; V2: euglycemia, high insulin; V3: hyperglycemia, low insulin) in random order. Glucose fluxes were measured with tracer-tracee clamp using [6,6-2H2] glucose before, during and after, 60 min of E at 65% VO2 max. By design, plasma glucose concentrations were higher in V3 than V1 and V2 (9.7±0.5, 5.2±0.1, 5.2±.0.1 mM respectively, p<0.05), while plasma insulin concentrations were higher in V2 than V1 and V3 (324.3±19.4, 129.3±9.3, 111.6±5.9 pM, p<0.05). Rd increased with E in all visits (p<0.05) and returned to pre-E values thereafter. EGP during E increased (p<0.05) in V1 and to a lesser extent in V3, but was unchanged in V2. To summarize, hyperinsulinemia, but not hyperglycemia inhibits E induced compensatory increase in EGP; both hyperinsulinemia and hyperglycemia augments increase in Rd with E albeit to different extents; Rd returns to pre-E values when E stops. Taken together, euglycemia coupled with low insulin appear to be the most favorable milieu for T1D during E.

D. Romeres: None. A. Basu: Research Support; Spouse/Partner; AstraZeneca. Research Support; Self; Novo Nordisk A/S. Advisory Panel; Self; Voluntis France. M. Schiavon: None. C. Cobelli: Research Support; Self; Sanofi-Aventis. Advisory Panel; Self; Novo Nordisk Inc.. C. Dalla Man: None. R. Basu: Research Support; Self; AstraZeneca.

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