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Research Article Free access | 10.1172/JCI115997

Increased rate of gluconeogenesis in type II diabetes mellitus. A 13C nuclear magnetic resonance study.

I Magnusson, D L Rothman, L D Katz, R G Shulman, and G I Shulman

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Magnusson, I. in: PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

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Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Katz, L. in: PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

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Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Shulman, G. in: PubMed | Google Scholar

Published October 1, 1992 - More info

Published in Volume 90, Issue 4 on October 1, 1992
J Clin Invest. 1992;90(4):1323–1327. https://doi.org/10.1172/JCI115997.
© 1992 The American Society for Clinical Investigation
Published October 1, 1992 - Version history
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Abstract

To quantitate hepatic glycogenolysis, liver glycogen concentration was measured with 13C nuclear magnetic resonance spectroscopy in seven type II diabetic and five control subjects during 23 h of fasting. Net hepatic glycogenolysis was calculated by multiplying the rate of glycogen breakdown by the liver volume, determined from magnetic resonance images. Gluconeogenesis was calculated by subtracting the rate of hepatic glycogenolysis from the whole body glucose production rate, measured using [6-3H]glucose. Liver glycogen concentration 4 h after a meal was lower in the diabetics than in the controls; 131 +/- 20 versus 282 +/- 60 mmol/liter liver (P < 0.05). Net hepatic glycogenolysis was decreased in the diabetics, 1.3 +/- 0.2 as compared to 2.8 +/- 0.7 mumol/(kg body wt x min) in the controls (P < 0.05). Whole body glucose production was increased in the diabetics as compared to the controls, 11.1 +/- 0.6 versus 8.9 +/- 0.5 mumol/(kg body wt x min) (P < 0.05). Gluconeogenesis was consequently increased in the diabetics, 9.8 +/- 0.7 as compared to 6.1 +/- 0.5 mumol/(kg body wt x min) in the controls (P < 0.01), and accounted for 88 +/- 2% of total glucose production as compared with 70 +/- 6% in the controls (P < 0.05). In conclusion: increased gluconeogenesis is responsible for the increased whole body glucose production in type II diabetes mellitus after an overnight fast.

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