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Original Articles

Predominant Role of Gluconeogenesis in Increased Hepatic Glucose Production in NIDDM

  1. Agostino Consoli,
  2. Nurjahan Nurjhan,
  3. Fabio Capani and
  4. John Gerich
  1. Departments of Medicine and Physiology, University of Pittsburgh, School of Medicine Pittsburgh, Pennsylvania Institute of Internal Medicine, University of Chieti Chieti, Italy
  1. Address correspondence and reprint requests to John E. Gerich, MD, Clinical Research Center, 3488 Presbyterian-University Hospital, 230 Lothrop Street, Pittsburgh, PA 15261.
Diabetes 1989 May; 38(5): 550-557. https://doi.org/10.2337/diab.38.5.550
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Abstract

Excessive hepatic glucose output is an important factor in the fasting hyperglycemia of non-insulindependent diabetes mellitus (NIDDM). To determine the relative contributions of gluconeogenesis and glycogenolysis in a quantitative manner, we applied a new isotopic approach, using infusions of [6-3H]glucose and [2-14C]acetate to trace overall hepatic glucose output and phosphoenolpyruvate gluconeogenesis in 14 postabsorptive NIDDM subjects and in 9 nondiabetic volunteers of similar age and weight. Overall hepatic glucose output was increased nearly twofold in the NIDDM subjects (22.7 ± 1.0 vs. 12.0 ± 0.6 μmol · kg−1 · min−1 in the nondiabetic volunteers, P < .001); phosphoenolpyruvate gluconeogenesis was increased more than threefold in the NIDDM subjects (12.7 ± 1.4 vs. 3.6 ± 0.4 μmol kg−1 min−1 in the nondiabetic subjects, P < .001) and was accompanied by increased plasma lactate, alanine, and glucagon concentrations (all P < .05). The increased phosphoenolpyruvate gluconeogenesis accounted for 89 ± 6% of the increase in overall hepatic glucose output in the NIDDM subjects and was significantly correlated with the fasting plasma glucose concentrations (r = .67, P < .01). Glycogenolysis, calculated as the difference between overall hepatic glucose output and phosphoenolpyruvate gluconeogenesis, was not significantly different in the NIDDM subjects (9.9 ± 0.06 μmol · kg−1 · min−1) and the nondiabetic volunteers (8.4 ± 0.3 μmol kg−1 · min−1). We conclude that increased gluconeogenesis is the predominant mechanism responsible for increased hepatic glucose output in NIDDM.

  • Received June 29, 1988.
  • Revision received November 1, 1988.
  • Accepted November 1, 1988.
  • Copyright © 1989 by the American Diabetes Association

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May 1989, 38(5)
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Predominant Role of Gluconeogenesis in Increased Hepatic Glucose Production in NIDDM
Agostino Consoli, Nurjahan Nurjhan, Fabio Capani, John Gerich
Diabetes May 1989, 38 (5) 550-557; DOI: 10.2337/diab.38.5.550

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Predominant Role of Gluconeogenesis in Increased Hepatic Glucose Production in NIDDM
Agostino Consoli, Nurjahan Nurjhan, Fabio Capani, John Gerich
Diabetes May 1989, 38 (5) 550-557; DOI: 10.2337/diab.38.5.550
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