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Am J Physiol Endocrinol Metab (November 26, 2002). doi:10.1152/ajpendo.00471.2002
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Articles in PresS, published online ahead of print November 26, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00471.2002
Submitted on October 30, 2002
Accepted on November 21, 2002

Direct Assessment of Muscle Glycogen Storage After Mixed Meals in Normal and Type 2 Diabetic Subjects

Peter E. Carey1, Jayne Halliday2, Johanna E. Snaar2, Peter Morris2, and Roy Taylor1*

1 Department of Diabetes and Metabolism, University of Newcastle-upon-Tyne, Newcastle-upon-Tyne, United Kingdom
2 Magnetic Resonance Centre, School of Physics and Astronomy, University of Nottingham, Nottingham, United Kingdom

* To whom correspondence should be addressed. E-mail: roy.taylor{at}ncl.ac.uk.

In order to understand the day to day pathophysiology of impaired muscle glycogen storage in type 2 diabetes, glycogen concentrations were measured before and after the consumption of sequential mixed meals (breakfast: 190.5 g carbohydrate, 41.0g fat, 28.8g protein, 1253 kcal; lunch: 203.3 g carbohydrate, 48.1g fat, 44.0g protein, 1497.5 kcal) using natural abundance 13C magnetic resonance spectroscopy. Subjects with diet controlled type 2 diabetes (n=9) and age- and BMI-matched non-diabetic controls (n=9) were studied. Mean fasting gastrocnemius glycogen concentration was significantly lower in the diabetic group (57.1 ± 3.6 vs. 68.9 ± 4.1mmol/l; p<0.05). Following the first meal mean glycogen concentration in the control group rose significantly from basal (97.1 ± 7.0 mmol/l at 240 min; p=0.005). After the second meal the high level of muscle glycogen concentration in the control group was maintained, with a further rise to 108.0 ± 11.6 mmol/l by 480 min. In the diabetic group the postprandial rise was markedly lower than that of the control group (65.9 ± 5.2 mmol/l at 240 min, p<0.005 and 70.8 ± 6.7 mmol/l at 480 min, p=0.01), despite considerably greater serum insulin levels (752.0 ± 109.0 vs. 372.3 ± 78.2 pmol/l at 300 min, p=0.013). This was associated with a significantly greater post-prandial hyperglycemia (10.8 ± 1.3 mmol/l versus 5.3 ± 0.2 mmol/l at 240 min, p<0.005). Basal muscle glycogen concentration correlated inversely with fasting blood glucose (r = -0.55, p<0.02) and fasting serum insulin (r = -0.57, p<0.02). The increment in muscle glycogen correlated with initial increment in serum insulin only in the control group (r = 0.87, p<0.002). This study quantitates for the first time the subnormal basal muscle glycogen concentration and the inadequate glycogen storage after meals in type 2 diabetes.




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