Abnormal renal and hepatic glucose metabolism in type 2 diabetes mellitus
Abnormal renal and hepatic glucose metabolism in type 2 diabetes mellitus
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DOI：
10.1172/jci2415
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发表时间：
1998-08-01
影响因子：
15.9
通讯作者：
Gerich, J
中科院分区：
文献类型：
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作者：
Meyer, C;Stumvoll, M;Gerich, J
在糖尿病动物中，肝脏和肾脏的葡萄糖释放均增加。尽管糖尿病患者中葡萄糖向循环中的总体释放增加，但尚未证实肝脏或肾脏过度释放葡萄糖。因此，进行本实验以评估肝和肾葡萄糖释放对2型糖尿病中发现的过度葡萄糖释放的相对贡献。使用同位素和平衡技术的组合来确定吸收后2型糖尿病受试者和年龄-体重匹配的非糖尿病志愿者中的总全身葡萄糖释放和肾葡萄糖释放，然后计算他们的肝脏葡萄糖释放为总的全身葡萄糖释放和肾脏葡萄糖释放之间的差，糖尿病受试者的肾脏葡萄糖释放增加近300（321+/-36 vs. 125+/-15 μ mol/min，P < 0.001），肝脏葡萄糖释放增加了30%（P = 0.03），但肝脏和肾脏葡萄糖释放的增量相当（分别为2.60+/-0.70 vs. 2.21+/-0.32，mu mol.kg（-1）.min（-1），P = 0.26）。糖尿病受试者的肾脏葡萄糖摄取显著增加（353 +/- 48 vs. 103 +/- 10 μ mol/min，P < 0.001），导致糖尿病受试者的肾脏葡萄糖净摄取（92 +/- 50 μ mol/ min）与非糖尿病受试者的净输出（21 +/- 14 μ mol/min，P = 0.043）。肾脏葡萄糖摄取与肾脏FFA摄取呈负相关（r =-0.51，P < 0.01），糖尿病组降低约60%（10.9+/-2.7 vs. 27.0+/-3.3 μ mol/min，P < 0.002），我们得出结论，在2型糖尿病中，肝脏和肾脏都有助于葡萄糖的过度产生，并且肾脏葡萄糖摄取显著增加。后者可能通过葡萄糖-脂肪酸循环抑制肾脏FFA的摄入，并解释了糖尿病肾脏中常见的糖原积聚。
Release of glucose by liver and kidney are both increased in diabetic animals, Although the overall release of glucose into the circulation is increased in humans with diabetes, excessive release of glucose by either their liver or kidney has not as yet been demonstrated. The present experiments were therefore undertaken to assess the relative contributions of hepatic and renal glucose release to the excessive glucose release found in type 2 diabetes, Using a combination of isotopic and balance techniques to determine total systemic glucose release and renal glucose release in postabsorptive type 2 diabetic subjects and age-weight-matched nondiabetic volunteers, their hepatic glucose release was then calculated as the difference between total systemic glucose release and renal glucose release, Renal glucose release was increased nearly 300% in diabetic subjects (321+/-36 vs. 125+/-15 mu mol/min, P < 0.001), Hepatic glucose release was increased similar to 30% (P = 0.03), but increments in hepatic and renal glucose release were comparable (2.60+/-0.70 vs. 2.21+/-0.32, mu mol.kg(-1).min(-1), respectively, P = 0,26). Renal glucose uptake was markedly increased in diabetic subjects (353 +/- 48 vs. 103 +/- 10 mu mol/min, P < 0.001), resulting in net renal glucose uptake in the diabetic subjects (92 +/- 50 mu mol/ min) versus a net output in the nondiabetic subjects (21 +/- 14 mu mol/min, P = 0.043). Renal glucose uptake was inversely correlated with renal FFA uptake (r = -0.51, P < 0.01), which was reduced by similar to 60% in diabetic subjects (10.9+/-2.7 vs. 27.0+/-3.3 mu mol/min, P < 0.002), We conclude that in type 2 diabetes, both liver and kidney contribute to glucose overproduction and that renal glucose uptake is markedly increased. The latter may suppress renal FFA uptake via a glucose-fatty acid cycle and explain the accumulation of glycogen commonly found in the diabetic kidney.