CONTRIBUTION OF HEPATIC GLYCOGENOLYSIS TO GLUCOSE-PRODUCTION IN HUMANS IN RESPONSE TO A PHYSIOLOGICAL INCREASE IN PLASMA-GLUCAGON CONCENTRATION
CONTRIBUTION OF HEPATIC GLYCOGENOLYSIS TO GLUCOSE-PRODUCTION IN HUMANS IN RESPONSE TO A PHYSIOLOGICAL INCREASE IN PLASMA-GLUCAGON CONCENTRATION
复制标题
DOI：
10.2337/diabetes.44.2.185
复制
发表时间：
1995-02-01
期刊：
影响因子：
7.7
通讯作者：
SHULMAN, GI
中科院分区：
文献类型：
--
作者：
MAGNUSSON, I;ROTHMAN, DL;SHULMAN, GI
在6名健康受试者（18-24岁，68-105 kg）中，在空腹过夜后，测量了血浆胰高血糖素浓度生理性增加期间净肝糖原分解对总体葡萄糖生成的贡献。输注胰高血糖素（类似于3 ng.kg（-1）.min（-1））、生长抑素（0.1 μ g.kg（-1）.min（-1））和胰岛素（0.9 pmol.kg（-1）min（-1））3小时。在此期间，使用C-13标记的核磁共振波谱法每隔15分钟测量一次肝糖原浓度，并通过磁共振图像评估肝脏体积。净肝糖原分解率计算为肝糖原浓度随时间的降低乘以肝体积。使用葡萄糖动力学的二室模型，根据[3-H-3]葡萄糖周转数据计算葡萄糖出现率（R（a））。输注开始时，血浆胰高血糖素浓度从136 +/- 18升至304 +/- 57 ng/l，血糖浓度从5.6 +/- 0.1升至10.4 +/- 0.9 mmol/l。平均基线R（a）为11.8 +/- 0.4 mu mol.kg（-1）.min（-1），在输注开始后迅速增加，在20-40 min后达到最高值，并在140 min时恢复至基线。肝糖原浓度几乎呈线性下降输注开始后2小时内（从基线时的300 +/- 19 mmol/l肝脏至t = 124 min时的192 +/- 20 mmol/l肝脏），计算的净肝糖原分解的平均速率为21.7 +/- 3.6 μ mol.kg（-1）.min（-1）。同一时期的平均R（a）为22.8 +/- 2.3 mu mol.kg（-1）.min（-1）。因此，净肝糖原分解占R（a）的93 ± 9%。总之，在对血浆胰高血糖素生理性增加的初始反应期间，1）净肝糖原分解几乎占肝葡萄糖产生的所有增加，2）胰高血糖素对肝葡萄糖产生的短暂效应不是由肝糖原储备消耗引起的。
The contribution of net hepatic glycogenolysis to overall glucose production during a physiological increment in the plasma glucagon concentration was measured in six healthy subjects (18-24 years, 68-105 kg) after an overnight fast. Glucagon (similar to 3 ng.kg(-1).min(-1)), somatostatin (0.1 mu g.kg(-1).min(-1)), and insulin (0.9 pmol.kg(-1) min(-1)) were infused for 3 h. Liver glycogen concentration was measured at 15-min intervals during this period using C-13-labeled nuclear magnetic resonance spectroscopy, and liver volume was assessed hom magnetic resonance images. The rate of net hepatic glycogenolysis was calculated horn the decrease in liver glycogen concentration over time, multiplied by the liver volume. The rate of glucose appearance (R(a)) was calculated from [3-H-3]glucose turnover data using a two-compartment model of glucose kinetics. Plasma glucagon concentration rose from 136 +/- 18 to 304 +/- 57 ng/l and plasma glucose concentration rose from 5.6 +/- 0.1 to 10.4 +/- 0.9 mmol/l on initiation of the infusions. Mean baseline R(a) was 11.8 +/- 0.4 mu mol.kg(-1).min(-1), increased rapidly after the beginning of the infusions, reaching its highest value after 20-40 min, and returned to baseline by 140 min. Liver glycogen concentration decreased almost linearly (from 300 +/- 19 mmol/l liver at baseline to 192 +/- 20 mmol/l liver at t = 124 min) during 2 h after the beginning of the infusions, and the calculated mean rate of net hepatic glycogenolysis was 21.7 +/- 3.6 mu mol.kg(-1).min(-1). Mean R(a) during the same time period was 22.8 +/- 2.3 mu mol.kg(-1).min(-1). Thus, net hepatic glycogenolysis accounted for 93 +/- 9% of R(a). In conclusion, during the initial response to a physiological increment in plasma glucagon, 1) net hepatic glycogenolysis accounts for virtually all of the increase in hepatic glucose production, and 2) glucagon's evanescent effect on hepatic glucose production is not caused by depletion of hepatic glycogen stores.