Effects of low-dose and high-dose glucagon on glucose production and gluconeogenesis in humans.
Effects of low-dose and high-dose glucagon on glucose production and gluconeogenesis in humans.
复制标题
低剂量和高剂量胰高血糖素对人类葡萄糖产生和糖异生的影响。
DOI：
10.1016/s0026-0495(00)90638-3
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Tayek,JA
中科院分区：
文献类型：
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作者：
Chhibber,VL;Soriano,C;Tayek,JA
血糖和乳酸盐中的质量同位素异构体的分析可用于估计肝脏的非葡萄糖异生（Gneo）、葡萄糖产生（GP），以及通过减法估计肝脏的非葡萄糖异生葡萄糖释放。在早上6点，18名正常受试者接受了7小时的[U-13 C6]葡萄糖预充恒定输注。在3小时基线期（禁食12小时）后，输注生长抑素、胰岛素、氢化皮质激素、生长激素（GH）和胰高血糖素4小时。以低剂量（n = 6）或高剂量（n = 6）浓度输注胰高血糖素4小时，并与单独空腹（n = 6）进行比较。低剂量胰高血糖素输注增加血浆胰高血糖素（64 ± 3 vs 44 ± 7 ng/L，低胰高血糖素vs基线）。GP高于基线水平（15.5 ± 0.5 vs 13.8 ± 0.5 μmol/kg/min，P <0.05），也高于单独禁食（11.5 ± 0.6 μmol/kg/min，P <0.05）。GP的升高是由于非糖异生性葡萄糖的释放与单独禁食相比增加了近一倍（8.3 ± 0.6 v4.7 ± 0.5 μmol/kg/min，P <0.01）。高剂量胰高血糖素输注（125 ± 25 ng/L）使GP高于基线水平（15.8 ± 0.6 vs 13.5 ± 0.5 μmol/kg/min，P <0.05），这也大于单独禁食（11.5 ± 0.6 μmol/kg/min，P <0.05）。GP的增加是由于Gneo（8.5 ± 0.5 v6.8 ± 0.7 μmol/kg/min，P <0.05）和非黄体生成性葡萄糖释放（7.4 ± 0.5 v4.7 ± 0.4 μmol/kg/min，P <0.05）增加所致。低剂量胰高血糖素仅通过刺激非糖异生葡萄糖释放增加GP。高剂量胰高血糖素通过增加Gneo和非葡萄糖异生葡萄糖释放来增加GP。
The analysis of mass isotopomers in blood glucose and lactate can be used to estimate gluconeogenesis (Gneo), glucose production (GP), and, by subtraction, nongluconeogentic glucose release by the liver. At 6 am, 18 normal subjects received a 7-hour primed constant infusion of [U-13C6] glucose. After a 3-hour baseline period (12 hours of fasting), somatostatin, insulin, hydrocortisome, growth hormone (GH), and glucagon were infused for 4 hours. Glucagon was infused at a low-dose (n = 6) or high-dose (n = 6) concentration for 4 hours and was compared with fasting alone (n = 6). Low-dose glucagon infusion increased plasma glucagon (64 ± 3 v 44 ± 7 ng/L, low glucagon v baseline). GP increased above baseline (15.5 ± 0.5 v 13.8 ± 0.5 μmol/kg/min, P < .05), which was also greater than fasting alone (11.5 ± 0.6 μmol/kg/min, P < .05). The elevation in GP was due to a near doubling of nongluconeogenic glucose release compared with fasting alone (8.3 ± 0.6 v 4.7 ± 0.5 μmol/kg/min, P < .01). High-dose glucagon infusion (125 ± 25 ng/L) increased GP above baseline (15.8 ± 0.6 v 13.5 ± 0.5 μmol/kg/min, P < .05), which was also greater than fasting alone (11.5 ± 0.6 μmol/kg/min, P < .05). The increase in GP was due to an increase in Gneo (8.5 ± 0.5 v 6.8 ± 0.7 μmol/kg/min, P < .05) and nonglutoneogenic glucose release (7.4 ± 0.5 v 4.7 ± 0.4 μmol/kg/min, P < .05) compared with fasting. Low-dose glucagon increases GP only by stimulation of nongluconeogenic glucose release. High-dose glucagon increases GP by an increase in both Gneo and nongluconeogenic glucose release.