Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California 90033, USA.
Am J Physiol Endocrinol Metab. 2010 Feb;298(2):E346-53. doi: 10.1152/ajpendo.00280.2009. Epub 2009 Nov 24.
The full impact of the liver, through both glucose production and uptake, on systemic glucose appearance cannot be readily studied in a classical glucose clamp because hepatic glucose metabolism is regulated not only by portal insulin and glucose levels but also portal glucose delivery (the portal signal). In the present study, we modified the classical glucose clamp by giving exogenous glucose through portal vein, the "portal glucose infusion (PoG)-glucose clamp", to determine the net hepatic effect on postprandial systemic glucose supply along with the measurement of whole body glucose disposal. By comparing systemic rate of glucose appearance (R(a)) with portal glucose infusion rate (PoG(inf)), we quantified "net hepatic glucose addition (NHGA)" in the place of endogenous glucose production determined in a regular clamp. When PoG-glucose clamps (n = 6) were performed in dogs at basal insulinemia and hyperglycemia ( approximately 150 mg/dl, portal and systemic), we measured consistently higher R(a) than PoG(inf) (4.2 +/- 0.6 vs. 2.9 +/- 0.6 mg x kg(-1) x min(-1) at steady state, P < 0.001) and thus positive NHGA at 1.3 +/- 0.1 mg x kg(-1) x min(-1), identifying net hepatic addition of glucose to portal exogenous glucose. In contrast, when PoG-glucose clamps (n = 6) were performed at hyperinsulinemia ( approximately 250 pmol/l) and systemic euglycemia (portal hyperglycemia due to portal glucose infusion), we measured consistently lower R(a) than PoG(inf) (13.1 +/- 2.4 vs. 14.3 +/- 2.4 mg x kg(-1) x min(-1), P < 0.001), and therefore negative NHGA at -1.1 +/- 0.1 mg x kg(-1) x min(-1), identifying a switch of the liver from net production to net uptake of portal exogenous glucose. Steady-state whole body glucose disposal was 4.1 +/- 0.5 and 13.0 +/- 2.4 mg x kg(-1) x min(-1), respectively, determined as in a classical glucose clamp. We conclude that the PoG-glucose clamp, simulating postprandial glucose entry and metabolism, enables simultaneous assessment of the net hepatic effect on postprandial systemic glucose supply as well as whole body glucose disposal in various animal models (rodents, dogs, and pigs) with established portal vein catheterization.
通过门静脉给予外源性葡萄糖的改良经典葡萄糖钳夹,即“门静脉葡萄糖输注(PoG)-葡萄糖钳夹”,我们可以在测量全身葡萄糖处置的同时,确定肝脏对餐后系统葡萄糖供应的净作用。通过比较系统葡萄糖生成率(R(a))与门静脉葡萄糖输注率(PoG(inf)),我们用外源性葡萄糖输注所代表的“净肝葡萄糖添加(NHGA)”取代了常规钳夹中测定的内源性葡萄糖生成。当在基础胰岛素血症和高血糖(约 150mg/dl,门静脉和全身)条件下对狗进行 PoG-葡萄糖钳夹(n=6)时,我们观察到稳态时 R(a)始终高于 PoG(inf)(4.2+/-0.6 比 2.9+/-0.6mg x kg(-1) x min(-1),P<0.001),因此存在 1.3+/-0.1mg x kg(-1) x min(-1)的净肝葡萄糖添加,表明门静脉外源性葡萄糖被肝脏净添加到门静脉中。相比之下,当在高胰岛素血症(约 250pmol/l)和全身血糖正常(由于门静脉葡萄糖输注导致的门静脉高血糖)条件下进行 PoG-葡萄糖钳夹(n=6)时,我们观察到 R(a)始终低于 PoG(inf)(13.1+/-2.4 比 14.3+/-2.4mg x kg(-1) x min(-1),P<0.001),因此存在-1.1+/-0.1mg x kg(-1) x min(-1)的净肝葡萄糖负摄取,表明肝脏从净生成转为净摄取门静脉外源性葡萄糖。稳态时全身葡萄糖处置分别为 4.1+/-0.5 和 13.0+/-2.4mg x kg(-1) x min(-1),通过经典葡萄糖钳夹测定。我们的结论是,PoG-葡萄糖钳夹模拟了餐后葡萄糖的输入和代谢,能够在各种动物模型(啮齿动物、狗和猪)中同时评估肝脏对餐后系统葡萄糖供应的净作用以及全身葡萄糖处置,这些动物模型均建立了门静脉导管插入术。