Fried R, Beckmann N, Keller U, Ninnis R, Stalder G, Seelig J
Department of Internal Medicine, University Hospital, Basel, Switzerland.
Am J Physiol. 1996 Jan;270(1 Pt 1):G14-9. doi: 10.1152/ajpgi.1996.270.1.G14.
Galactose is incorporated by a different metabolic pathway than glucose. Its contribution to glycogen synthesis has not been studied in humans. We administered galactose (0.5 g/kg iv) to overnight-fasted normal human volunteers and examined its effects on hepatic glycogen synthesis and hepatic glucose output (HGO). Hepatic glycogenesis was assessed noninvasively, determining glycogen concentration by 13C magnetic resonance spectroscopy (MRS) and liver volume by magnetic resonance imaging. HGO was determined by [6,6-2H2]glucose and gluconeogenesis calculated by adding the amount of hepatic glycogenesis to the HGO. After galactose administration, liver glycogen concentration (baseline 254 +/- 11 mmol/l) decreased in the first 45 min to 207 +/- 15 mmol/l (P < 0.05) and increased thereafter to 313 +/- 7 mmol/l (P < 0.01). Net hepatic glycogenesis was 101 +/- 12 mmol over 150 min. HGO (baseline 14.3 +/- 1.9 mumol.kg-1.min-1) increased threefold in the first 15 min and then returned to baseline. The average rate of gluconeogenesis was 12.3 mumol.kg-1.min-1. Intravenous galactose leads to an increase in hepatic glycogen and hepatic glucose output in normal humans. Competitive inhibition of UDP-glucose pyrophosphorylase by UDP-galactose could explain the apparent glycogenolysis observed early after galactose administration. 13C MRS in combination with a stable isotope tracer is a noninvasive and safe method to study hepatic carbohydrate metabolism in humans.
半乳糖通过与葡萄糖不同的代谢途径被摄取。其对糖原合成的贡献尚未在人体中进行研究。我们对过夜禁食的正常人类志愿者静脉注射半乳糖（0.5 g/kg），并检查其对肝糖原合成和肝葡萄糖输出（HGO）的影响。通过13C磁共振波谱法（MRS）测定糖原浓度，通过磁共振成像测定肝脏体积，以非侵入性方式评估肝糖原生成。通过[6,6-2H2]葡萄糖测定HGO，并通过将肝糖原生成量与HGO相加来计算糖异生。注射半乳糖后，肝脏糖原浓度（基线为254±11 mmol/l）在最初45分钟内降至207±15 mmol/l（P<0.05），此后升至313±7 mmol/l（P<0.01）。150分钟内肝糖原净生成量为101±12 mmol。HGO（基线为14.3±1.9 μmol·kg-1·min-1）在最初15分钟内增加了两倍，然后恢复到基线水平。糖异生的平均速率为12.3 μmol·kg-1·min-1。静脉注射半乳糖可导致正常人体内肝糖原和肝葡萄糖输出增加。UDP-半乳糖对UDP-葡萄糖焦磷酸化酶的竞争性抑制可以解释在注射半乳糖后早期观察到的明显糖原分解现象。13C MRS与稳定同位素示踪剂相结合是研究人体肝脏碳水化合物代谢的一种非侵入性且安全方法。
