Direct assessment of muscle glycogen storage after mixed meals in normal and type 2 diabetic subjects
Direct assessment of muscle glycogen storage after mixed meals in normal and type 2 diabetic subjects
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DOI：
10.1152/ajpendo.00471.2002
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发表时间：
2003-04-01
影响因子：
5.1
通讯作者：
Taylor, R
中科院分区：
文献类型：
--
作者：
Carey, PE;Halliday, J;Taylor, R
为了了解 2 型糖尿病中肌糖原储存受损的日常病理生理学，我们在连续食用混合膳食（早餐：190.5 g 碳水化合物、41.0 g 脂肪、28.8 g 蛋白质、1,253 kcal；午餐：203.3 g 碳水化合物、48.1 g 脂肪、44.0 g 蛋白质、1,497.5 kcal）之前和之后测量了糖原浓度，方法是使用天然丰度 C-13 磁共振波谱。对饮食控制的 2 型糖尿病受试者 (n = 9) 和年龄和体重指数匹配的非糖尿病对照受试者 (n = 9) 进行了研究。糖尿病组的平均空腹腓肠肌糖原浓度显着较低（57.1 +/- 3.6 vs. 68.9 +/- 4.1 mmol/l；P < 0.05）。第一餐后，对照组的平均糖原浓度较基础值显着升高（240 分钟时为 97.1 +/- 7.0 mmol/l；P = 0.005）。第二餐后，对照组的肌糖原浓度维持在高水平，并在480分钟时进一步升至108.0+/-11.6mmol/l。在糖尿病组中，尽管血清胰岛素水平相当高（752.0 +/- 109.0 vs. 372.3 +/-），但餐后升高明显低于对照组（240 分钟时为 65.9 +/- 5.2 mmol/l，P < 0.005，480 分钟时为 70.8 +/- 6.7 mmol/l，P = 0.01）。 300 分钟时为 78.2 pmol/l，P = 0.013）。这与显着较高的餐后高血糖相关（240 分钟时为 10.8 +/- 1.3 对比 5.3 +/- 0.2 mmol/l，P < 0.005）。基础肌糖原浓度与空腹血糖（r = -0.55，P < 0.02）和空腹血清胰岛素（r = - 0.57，P < 0.02）呈负相关。仅在对照组中，肌糖原的增加与血清胰岛素的初始增加相关（r = 0.87，P < 0.002）。这项研究首次量化了 2 型糖尿病患者基础肌糖原浓度低于正常水平和餐后糖原储存不足的情况。
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 C-13 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.