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Original Articles

Contribution of Abnormal Muscle and Liver Glucose Metabolism to Postprandial Hyperglycemia in NIDDM

  1. Asimina Mitrakou,
  2. David Kelley,
  3. Thiemo Veneman,
  4. Trond Jenssen,
  5. Thomas Pangburn,
  6. James Reilly and
  7. John Gerich
  1. Clinical Research Center, Departments of Medicine, Physiology, and Surgery, University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania
  1. Address correspondence and reprint requests to John E. Gerich, MD, University of Pittsburgh, Clinical Research Center, 3488 Presbyterian-University Hospital, Pittsburgh, PA 15261.
Diabetes 1990 Nov; 39(11): 1381-1390. https://doi.org/10.2337/diab.39.11.1381
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Abstract

To assess the role of muscle and liver in the pathogenesis of postprandial hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM), we administered an oral glucose load enriched with [14C]glucose to 10 NIDDM subjects and 10 age- and weight-matched nondiabetic volunteers and compared muscle glucose disposal by measuring forearm balance of glucose, lactate, alanine, O2, and CO2 (with forearm calorimetry). In addition, we used the dual-lable isotope method to compare overall rates of glucose appearance (Ra) and disappearance (Rd), suppression of endogenous glucose output, and splanchnic glucose sequestration. During the initial 1–1.5 h after glucose ingestion, plasma glucose increased by ∼8 mM in NIDDM vs. ∼3 mM in nondiabetic subjects (P < 0.01); overall glucose Ra was nearly 11 g greater in NIDDM than nondiabetic subjects (45.1 ± 2.3 vs. 34.4 ± 1.5 g, P < 0.01), but glucose Rd was not significantly different in NIDDM (35.1 ± 2.4 g) and nondiabetic (33.3 ± 2.7 g) subjects. The greater overall glucose Ra of NIDDM subjects was due to 6.8 g greater endogenous glucose output (13.7 ± 1.1 vs. 6.8 ± 1.0 g, P < 0.01) and 3.8 g less oral glucose splanchnic sequestration of the oral load (31.4 ± 1.5 vs. 27.5 ± 0.9 g, P < 0.05). Although glucose taken up by muscle was not significantly different in NIDDM and nondiabetic subjects (39.3 ± 3.5 vs. 41.0 ± 2.5 g/5 h), a greater amount of the glucose taken up by muscle in NIDDM was released as lactate and alanine (11.7 ± 1.0 vs. 5.2 ± 0.3 g in nondiabetic subjects, P < 0.01), and less was stored (11.7 ± 1.3 vs. 16.9 ± 1.5 g, P < 0.05). We conclude that increased systemic glucose delivery, due primarily to reduced suppression of endogenous hepatic glucose output and, to a lesser extent, reduced splanchnic glucose sequestration, is the predominant factor responsible for postprandial hyperglycemia in NIDDM.

  • Received November 6, 1989.
  • Revision received June 27, 1990.
  • Accepted June 27, 1990.
  • Copyright © 1990 by the American Diabetes Association

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November 1990, 39(11)
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Contribution of Abnormal Muscle and Liver Glucose Metabolism to Postprandial Hyperglycemia in NIDDM
Asimina Mitrakou, David Kelley, Thiemo Veneman, Trond Jenssen, Thomas Pangburn, James Reilly, John Gerich
Diabetes Nov 1990, 39 (11) 1381-1390; DOI: 10.2337/diab.39.11.1381

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Contribution of Abnormal Muscle and Liver Glucose Metabolism to Postprandial Hyperglycemia in NIDDM
Asimina Mitrakou, David Kelley, Thiemo Veneman, Trond Jenssen, Thomas Pangburn, James Reilly, John Gerich
Diabetes Nov 1990, 39 (11) 1381-1390; DOI: 10.2337/diab.39.11.1381
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