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Research Article Free access | 10.1172/JCI2415

Abnormal renal and hepatic glucose metabolism in type 2 diabetes mellitus.

C Meyer, M Stumvoll, V Nadkarni, J Dostou, A Mitrakou, and J Gerich

Departments of Medicine and Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642, USA.

Find articles by Meyer, C. in: PubMed | Google Scholar

Departments of Medicine and Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642, USA.

Find articles by Stumvoll, M. in: PubMed | Google Scholar

Departments of Medicine and Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642, USA.

Find articles by Nadkarni, V. in: PubMed | Google Scholar

Departments of Medicine and Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642, USA.

Find articles by Dostou, J. in: PubMed | Google Scholar

Departments of Medicine and Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642, USA.

Find articles by Mitrakou, A. in: PubMed | Google Scholar

Departments of Medicine and Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642, USA.

Find articles by Gerich, J. in: PubMed | Google Scholar

Published August 1, 1998 - More info

Published in Volume 102, Issue 3 on August 1, 1998
J Clin Invest. 1998;102(3):619–624. https://doi.org/10.1172/JCI2415.
© 1998 The American Society for Clinical Investigation
Published August 1, 1998 - Version history
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Abstract

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 micromol/min, P < 0.001). Hepatic glucose release was increased approximately 30% (P = 0.03), but increments in hepatic and renal glucose release were comparable (2.60+/-0.70 vs. 2.21+/-0.32, micromol.kg-1.min-1, respectively, P = 0.26). Renal glucose uptake was markedly increased in diabetic subjects (353+/-48 vs. 103+/-10 micromol/min, P < 0.001), resulting in net renal glucose uptake in the diabetic subjects (92+/-50 micromol/ min) versus a net output in the nondiabetic subjects (21+/-14 micromol/min, P = 0.043). Renal glucose uptake was inversely correlated with renal FFA uptake (r = -0.51, P < 0.01), which was reduced by approximately 60% in diabetic subjects (10. 9+/-2.7 vs. 27.0+/-3.3 micromol/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.

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