Stumvoll M, Meyer C, Kreider M, Perriello G, Gerich J
Medizinische Klinik, Eberhard-Karls-Universität, Tübingen, Germany.
Metabolism. 1998 Oct;47(10):1227-32. doi: 10.1016/s0026-0495(98)90328-6.
Glutamine is an important gluconeogenic amino acid in postabsorptive humans. To assess the effect of glucagon on renal and hepatic glutamine gluconeogenesis, we infused six normal healthy postabsorptive subjects with glucagon at a rate chosen to produce circulating glucagon concentrations found during hypoglycemia and, using a combination of isotopic and net balance techniques, determined the systemic, renal, and hepatic glucose release and renal and hepatic production of glucose from glutamine. Infusion of glucagon increased systemic and hepatic glucose release (both P < .02), but had no effect on renal glucose release (P = .26). Systemic and hepatic glutamine gluconeogenesis increased from 0.45 +/- 0.3 and 0.11 +/- 0.02 micromol x kg(-1) x min(-1), respectively, to 0.61 +/- 0.04 (P = .002) and 0.31 +/- 0.03 micromol x kg(-1) x min(-1) (P = .001), respectively, whereas renal glutamine gluconeogenesis was unchanged (from 0.33 +/- 0.03 to 0.30 +/- 0.04 micromol x kg(-1) x min(-1), P = .20). The hepatic contribution to systemic glutamine gluconeogenesis increased from 25.2% +/- 6.2% to 51.6% +/- 5.5% (P = .002), while that of the kidney decreased from 74.8% +/- 6.2% to 48.4% +/- 5.5% (P = .003). Glucagon had no effect on the renal net balance, fractional extraction, or uptake and release of either glucose or glutamine. We thus conclude that glucagon stimulates glutamine gluconeogenesis in normal postabsorptive humans, predominantly due to an increase in hepatic glutamine conversion to glucose. Thus, under certain conditions such as counterregulation of hypoglycemia, the liver may be an important site of glutamine gluconeogenesis.
谷氨酰胺是空腹状态下人体中一种重要的糖异生氨基酸。为评估胰高血糖素对肾脏和肝脏谷氨酰胺糖异生的影响，我们以能产生低血糖时循环中胰高血糖素浓度的速率，给6名正常健康的空腹受试者输注胰高血糖素，并结合同位素和净平衡技术，测定全身、肾脏和肝脏的葡萄糖释放以及谷氨酰胺的肾脏和肝脏葡萄糖生成。输注胰高血糖素增加了全身和肝脏的葡萄糖释放（两者P <.02），但对肾脏葡萄糖释放无影响（P =.26）。全身和肝脏的谷氨酰胺糖异生分别从0.45±0.3和0.11±0.02微摩尔·千克⁻¹·分钟⁻¹增加到0.61±0.04（P =.002）和0.31±0.03微摩尔·千克⁻¹·分钟⁻¹（P =.001），而肾脏谷氨酰胺糖异生未改变（从0.33±0.03到0.30±0.04微摩尔·千克⁻¹·分钟⁻¹，P =.20）。肝脏对全身谷氨酰胺糖异生的贡献从25.2%±6.2%增加到51.6%±5.5%（P =.002），而肾脏的贡献从74.8%±6.2%降至48.4%±5.5%（P =.003）。胰高血糖素对肾脏的净平衡、分数提取或葡萄糖或谷氨酰胺的摄取与释放均无影响。因此我们得出结论，胰高血糖素刺激正常空腹人体的谷氨酰胺糖异生，主要是由于肝脏将谷氨酰胺转化为葡萄糖增加。所以，在某些情况下，如低血糖的对抗调节，肝脏可能是谷氨酰胺糖异生的重要场所。
