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Updated: Jul 13, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes:
K Chokkalingam1,2, K Tsintzas1, J E M Snaar3
1Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, University of Nottingham, Nottingham, UK.
Aims/Hypothesis:
We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers.
Methods:
We studied seven men with type 1 diabetes (mean +/- SEM diabetes duration 10 +/- 2 years, age 33 +/- 3 years, BMI 24 +/- 1 kg/m(2), HbA(1c) 8.1 +/- 0.2% and VO(2) peak 43 +/- 2 ml [kg lean body mass](-1) min(-1)) and five non-diabetic controls (mean +/- SEM age 30 +/- 3 years, BMI 22 +/- 1 kg/m(2), HbA(1c) 5.4 +/- 0.1% and VO(2) peak 52 +/- 4 ml [kg lean body mass](-1) min(-1), before and after a standardised breakfast and after three bouts (EX1, EX2, EX3) of 40 min of cycling at 60% VO(2) peak. (13)C Magnetic resonance spectroscopy of liver glycogen was acquired in a 3.0 T magnet using a surface coil. Whole-body substrate oxidation was determined using indirect calorimetry.
Results:
Blood glucose and serum insulin concentrations were significantly higher (p < 0.05) in the fasting state, during the postprandial period and during EX1 and EX2 in subjects with type 1 diabetes compared with controls. Serum insulin concentration was still different between groups during EX3 (p < 0.05), but blood glucose concentration was similar. There was no difference between groups in liver glycogen concentration before or after the three bouts of exercise, despite the relative hyperinsulinaemia in type 1 diabetes. There were also no differences in substrate oxidation rates between groups.
Conclusions/Interpretation:
In patients with type 1 diabetes, hyperinsulinaemic and hyperglycaemic conditions during moderate exercise did not suppress hepatic glycogen concentrations. These findings do not support the hypothesis that exercise-induced hypoglycaemia in patients with type 1 diabetes is due to suppression of hepatic glycogen mobilisation.
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