FAILURE OF GLUCAGON SUPPRESSION CONTRIBUTES TO POSTPRANDIAL HYPERGLYCEMIA IN IDDM
FAILURE OF GLUCAGON SUPPRESSION CONTRIBUTES TO POSTPRANDIAL HYPERGLYCEMIA IN IDDM
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DOI：
10.1007/s001250050290
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发表时间：
1995-03-01
期刊：
影响因子：
8.2
通讯作者：
RIZZA, R
中科院分区：
文献类型：
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作者：
DINNEEN, S;ALZAID, A;RIZZA, R
摄入碳水化合物会导致非糖尿病患者胰高血糖素浓度下降，而糖尿病患者则不会。为了确定餐后胰高血糖素缺乏抑制是否会导致高血糖，以及其机制，9名胰岛素依赖型糖尿病（IDDM）患者分别摄入了50克含[2-H-3]和[6-H-3]葡萄糖的葡萄糖。[6-C-14]葡萄糖、胰岛素和低剂量生长抑素在两种情况下以相同的速率静脉滴注。基础胰高血糖素输注在葡萄糖摄入的同时（“恒定胰高血糖素”）或2小时后（“抑制胰高血糖素”）开始。这导致在抑制的前2小时胰高血糖素浓度低于胰高血糖素恒定研究期间（63 +/- vs 108 +/- 2 pg/ mi）。缺乏胰高血糖素抑制导致餐后葡萄糖浓度升高（10.3 +/- 0.9 vs 8.1 +/- 0.7 mmol/l） （p < 0.01）和更大的综合血糖反应（p < 0.02）。葡萄糖的过度升高是由于在恒定期间餐后肝脏葡萄糖释放率高于抑制胰高血糖素研究期间（g < 0.02），无论使用[6-H-3]葡萄糖（2.6 +/- 0.2 vs 2.0 +/- 0.2 mmol）。kg（-1）每6小时)或[2-H-3]葡萄糖（3.0 +/- 0.3 vs 2.4 +/- 0.2 mmol）。Kg (-1) / 6 h)作为示踪剂。葡萄糖消失、初始内脏葡萄糖清除和肝脏葡萄糖循环在两种情况下没有差异。因此，目前的研究表明，缺乏餐后胰高血糖素抑制，通过增加肝脏葡萄糖释放，有助于IDDM患者的高血糖。
Carbohydrate ingestion results in a fall in glucagon concentration in non-diabetic but not in diabetic individuals. To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-H-3] glucose and [6-H-3] glucose on two occasions. [6-C-14] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions. A basal glucagon infusion was started either at the same time (''constant glucagon'') or 2 h following (''suppressed glucagon'') glucose ingestion. This resulted in lower (p < 0.001) glucagon concentrations during the first 2 h of the suppressed than during the constant glucagon study days (63 +/- vs 108 +/- 2 pg/ mi). Lack of suppression of glucagon led to higher (p < 0.01) postprandial glucose concentrations (10.3 +/- 0.9 vs 8.1 +/- 0.7 mmol/l) and a greater (p < 0.02) integrated glycaemic response. The excessive rise in glucose was due to higher (g < 0.02) rates of postprandial hepatic glucose release during the constant than during the suppressed glucagon study days, whether measured using either [6-H-3] glucose (2.6 +/- 0.2 vs 2.0 +/- 0.2 mmol . kg(-1) per 6 h) or [2-H-3] glucose (3.0 +/- 0.3 vs 2.4 +/- 0.2 mmol . kg(-1) per 6 h) as the meal tracer. Glucose disappearance, initial splanchnic glucose clearance and hepatic glucose cycling did not differ on the two occasions. Thus, the present studies demonstrate that lack of postprandial suppression of glucagon, by increasing hepatic glucose release, contributes to hyperglycaemia in subjects with IDDM.