Published in:
01-09-2007 | Article
Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study
Authors:
K. Chokkalingam, K. Tsintzas, J. E. M. Snaar, L. Norton, B. Solanky, E. Leverton, P. Morris, P. Mansell, I. A. Macdonald
Published in:
Diabetologia
|
Issue 9/2007
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Abstract
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/m2, HbA1c 8.1 ± 0.2% and VO2 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/m2, HbA1c 5.4 ± 0.1% and VO2 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% VO2 peak. 13C 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.