Direct assessment of muscle glycogen storage after mixed meals in normal and type 2 diabetic subjects

1  Department of Diabetes and Metabolism, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH; and 2  Magnetic Resonance Centre, School of Physics and Astronomy, University of Nottingham, Nottingham NG7 2RD, United Kingdom To understand the day-to-day pathophysiology of impaired muscle gl...

Full description

Saved in:
Bibliographic Details
Published inAmerican journal of physiology: endocrinology and metabolism Vol. 284; no. 4; pp. E688 - E694
Main Authors Carey, P. E, Halliday, J, Snaar, J. E. M, Morris, P. G, Taylor, R
Format Journal Article
LanguageEnglish
Published United States 01.04.2003
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:1  Department of Diabetes and Metabolism, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH; and 2  Magnetic Resonance Centre, School of Physics and Astronomy, University of Nottingham, Nottingham NG7 2RD, United Kingdom 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, 41.0 g fat, 28.8 g protein, 1,253 kcal; lunch: 203.3 g carbohydrate, 48.1 g fat, 44.0 g protein, 1,497.5 kcal) by use of natural abundance 13 C magnetic resonance spectroscopy. Subjects with diet-controlled type 2 diabetes ( n  = 9) and age- and body mass index-matched nondiabetic controls ( n  = 9) were studied. Mean fasting gastrocnemius glycogen concentration was significantly lower in the diabetic group (57.1   ± 3.6 vs. 68.9 ± 4.1 mmol/l; P  < 0.05). After 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 postprandial hyperglycemia (10.8 ± 1.3 vs. 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. type 2 diabetes; magnetic resonance spectroscopy; insulin resistance
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0193-1849
1522-1555
DOI:10.1152/ajpendo.00471.2002