Wi J K, Kim J K, Youn J H
Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033, USA.
Am J Physiol. 1996 May;270(5 Pt 1):E752-8. doi: 10.1152/ajpendo.1996.270.5.E752.
Postabsorptive hepatic glucose output (HGO) was estimated in normal (n = 9) and streptozotocin (STZ) diabetic rats after a 6-h [3-3H]glucose infusion. In diabetic rats, HGO was estimated at ambient (n = 12) or normal (achieved via phlorizin infusion; n = 9) glucose concentrations. HGO was not statistically different between normal and diabetic rats (63 +/- 3 vs. 77 +/- 10 mumol.kg-1.min-1; P > 0.05). HGO was also normal in diabetic rats even when plasma glucose was normalized with phlorizin infusion (71 +/- 5 vs. 63 +/- 3 mumol.kg-1.min-1; P > 0.05). In contrast, peripheral glucose uptake, when estimated at matched euglycemia, was lower by approximately 25% in diabetic than in normal rate (46 +/- 6 vs. 62 +/- 3 mumol.kg-1.min-1; P < 0.01). In addition, acute changes in plasma glucose concentrations did not have significant effects on HGO or peripheral glucose uptake in diabetic rats (P > 0.05), resulting in markedly decreased glucose clearance at ambient hyperglycemia (P < 0.001). In conclusion, postabsorptive HGO was not elevated in a majority (17 of 21) of STZ diabetic rats with severe hyperglycemia and therefore was not responsible for postabsorptive hyperglycemia. Our data suggest that an impairment in the ability of glucose to regulate peripheral glucose uptake or HGO develops in STZ diabetes and contributes to postabsorptive hyperglycemia.
在正常大鼠（n = 9）和链脲佐菌素（STZ）诱导的糖尿病大鼠中，经6小时[3-3H]葡萄糖输注后，评估空腹状态下的肝葡萄糖输出（HGO）。对于糖尿病大鼠，在环境葡萄糖浓度（n = 12）或正常葡萄糖浓度（通过输注根皮苷实现；n = 9）下评估HGO。正常大鼠和糖尿病大鼠之间的HGO无统计学差异（63±3 vs. 77±10 μmol·kg-1·min-1；P>0.05）。即使通过输注根皮苷使糖尿病大鼠的血糖正常化，其HGO仍正常（71±5 vs. 63±3 μmol·kg-1·min-1；P>0.05）。相比之下，在匹配的正常血糖水平下评估时，糖尿病大鼠的外周葡萄糖摄取比正常大鼠低约25%（46±6 vs. 62±3 μmol·kg-1·min-1；P<0.01）。此外，血浆葡萄糖浓度的急性变化对糖尿病大鼠的HGO或外周葡萄糖摄取无显著影响（P>0.05），导致在环境高血糖时葡萄糖清除率显著降低（P<0.）。总之，在大多数（21只中的17只）严重高血糖的STZ糖尿病大鼠中，空腹状态下的HGO并未升高，因此不是空腹高血糖的原因。我们的数据表明，在STZ糖尿病中，葡萄糖调节外周葡萄糖摄取或HGO的能力受损，并导致空腹高血糖。
