K Chokkalingam1,2, K Tsintzas1, J E M Snaar3, L Norton1, B Solanky3, E Leverton3, P Morris3, P Mansell2, I A Macdonald4,5. 1. Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, University of Nottingham, Nottingham, UK. 2. Queen's Medical Centre, Nottingham, UK. 3. Sir Peter Mansfield Magnetic Resonance Centre, University of Nottingham, Nottingham, UK. 4. Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, University of Nottingham, Nottingham, UK. Ian.macdonald@nottingham.ac.uk. 5. School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, Derby Road, Nottingham, NG7 2UH, UK. Ian.macdonald@nottingham.ac.uk.
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/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.
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.
Authors: J H Hwang; G Perseghin; D L Rothman; G W Cline; I Magnusson; K F Petersen; G I Shulman Journal: J Clin Invest Date: 1995-02 Impact factor: 14.808